Friday, July 8, 2016

The Whiteness of Whiteness or White Supremacy as White lunacy or why you think you sane when you crazy (denial)


When I announced the title of my recovery manual How to Recover from the Addiction to White Supremacy, people told me not to entitle the book as such but call it How to Recover from White Lunacy because lunacy is deeper than supremacy. Supposedly, supremacy suggests a certain level of sanity but according to my advisers and the elders white people are simply insane and supremacy is only a part of their insanity. Elijah Muhammad asked us why don't white people want us to have social equality with them? Answer: because if we have social equality with them we will discover how nasty and filthy they are. Was Elijah right? Yes! But Jesus told us even more about them. He said they are liars and murderers who abide not in the truth. He said if God were your Father you would love me but you seek to kill me because I tell you the truth. Has not America killed her truth tellers, e.g., JFK, RFK, MLK, MX, et al.?

But let's get to the whiteness of whiteness! What do I mean? I mean these people are so absorbed in their mythology of whiteness they don't have a clue how damaging their whiteness is to themselves and others, therefore they are qualified for admission to the mental institution. They condemn any and everything Black people express in our attempt to communicate with them our feelings of humanity. We say Black Lives Matter and they know Black lives don't matter to them for they treat their dogs better than they treat us, so BLM means nothing to them thus they ridicule it and wish we would dispense the idea that our lives matter, for all lives matter in their sick minds while the news shows them nightly how little Black lives matter when pigs kill our men in front of our women and children, and often kill our children and women. And then they are bewildered why we cry Black Lives Matter. Of course, Baldwin said they live in an airless room and furthermore the idea of white supremacy has led them to rationalizations so fantastic it approaches the pathological!

They kill us at the drop of a hat, and then when we kill them they are utterly astounded that we would have the nerve to harm precious white flesh, and yet they will flip the subject to why we kill each other as if they haven't taught us to hate each other in the same manner they hate us. Every institution in American society suggests we must hate ourselves and love them. Every image of a woman is that of a white woman or a almost white Black woman. One need only look at the Rap videos to see how often a Black skinned woman is projected as the object of beauty, even though they know and we know the Black woman's body is the true standard of beauty since the beginning of time.

So our women are brainwashed to hate their black skin from Africa to Jamaica--bleaching cream is imported into Africa by the tons so women can emulate the European standard of beauty, and the same is true in India and China. Yes, White lunacy is global and the addiction to white lunacy is global. As is taught in drug and alcohol recovery, addiction is cunning and vile. One can have a relapse at the drop of a hat, the slip of a tongue can reveal the residue of white lunacy even while the addict claims recovery.

The solution to recovery from the addiction to the whiteness of whiteness or white lunacy is long term recovery to engender neuroplasticity that will allow the brain cells to change due to a new environment.

The more we try to make them part of the human family, the more they reveal themselves as part of the animal family of beasts and predators of the worse jungle variety. They want us to stop killing each other but who taught us to kill? They did and as we speak they are killing around the world for nothing. They cannot tell us why they are still killing in Iraq, Afghanistan, Syria, Yemen, Somalia, etc.

For that matter, can they tell us why they kill a human being for selling single cigarettes, CDs, DVDs,
a defective tail light, signal light, for going to the store for a soda, for being mentally ill? Why would you kill the mentally ill? It is because you are addicted to murder under the color of law. We cannot have a trillion dollar military budget to kill around the world, including a president who checks off a murder list weekly, then expect no blow back? What did James Baldwin tell you, "The murder of my child will not make your child safe!"
 --Marvin X, How to Recover from the Addiction to White Supremacy, Black Bird Press, Berkeley CA.

 

 Neuroplasticity

NEUROPLASTICITY

Information in the brain is transmitted from neuron to neuron through specialized connections called synapses. A synapse between two neurons is made up of presynaptic and postsynaptic terminals, which are separated by a synaptic cleft. The presynaptic terminal is filled with small vesicles containing chemical neurotransmitters, and the postsynaptic terminal consists of receptors specific for these neurochemicals. Neurons carry information in the form of an electrical impulse called an action potential that is initiated at the cell body and travels down the axon. At the synapse, an action potential causes the voltage-dependent release of neurotransmitter-filled vesicles, thereby converting an electrical impulse into a chemical signal. Neurotransmitters diffuse across the synaptic cleft, where they bind to receptors and generate an electrical signal in the postsynaptic neuron. The postsynaptic cell will then, in turn, fire an action potential if the sum of all its synapses reaches an electrical threshold for firing. Since a neuron can receive synapses from many different presynaptic cells, each cell is able to integrate information from varied sources before passing along the information in the form of an electrical code. The ability of neurons to modify the strength of existing synapses, as well as form new synaptic connections, is called neuroplasticity. It is believed that neuroplasticity may be the underlying cellular mechanism for the brain's ability to encode information during learning. In theory, this is how information is stored as memory.
Defined in this way, neuroplasticity includes changes in strength of mature synaptic connections, as well as the formation and elimination of synapses in adult and developing brains. This encompasses a vast field of research, and similar processes may also occur at peripheral synapses, where much of the pioneering studies on synaptic transmission first took place. In addition, neuroplasticity includes the regrowth (or sprouting) of new synaptic connections following central nervous system injury; following stroke, for example.
The notion that the brain can store information by modifying synaptic connections is not a new one. In fact, Santiago Ramon y Cajal (a founder of modern neuroscience) expressed this theory in 1894, three years before Charles Sherrington coined the term synapse to describe the connections made between neurons. In the late 1940s the neuroplasticity model was advanced by Jerzy Konorski, who used the word plasticity to describe "permanent functional transformations," and Donald Hebb, who ascribed testable physiologic characteristics to synaptic plasticity. However, experimental evidence that synapses are capable of long-lasting changes in synaptic strength did not come until the early 1970s, when Timothy Bliss and Terry Lomo described an increase in the synaptic strength of neurons in the mammalian hippocampus (a region of the brain critical for some forms of memory) following electrical stimulation. They termed this increase long-lasting potentiation, now referred to as long-term potentiation (LTP).
Changes in synaptic strength proved to be bidirectionally modifiable (they increase and decrease in strength) as Serena Dudek and Mark Bear first demonstrated in 1992 by recording activity-driven, long-term depression (LTD) in the hippocampus. The evidence that learning and memory are based on these long-lasting changes in synaptic strength is substantial, but still incomplete. However, defining the molecular constituents in the mechanistic pathway leading from synaptic activity to plasticity continues to strengthen the evidence linking neuroplasticity with learning and memory. In addition, resolving the molecular mechanisms underlying synaptic modification should lead to targets for clinical intervention in eliminating age-related memory loss or synaptic loss following brain damage by enhancing new synaptic connections.

Mechanisms of plasticity

Synaptic plasticity can occur at either the presynaptic or postsynaptic terminal. Modifications to the presynaptic terminal affect the release of neurotransmitters. As the action potential invades the presynaptic terminal, it activates voltage-gated calcium channels that conduct calcium ions into the presynaptic terminal. This rise in intracellular calcium triggers the exocytosis of vesicles (fusion with the plasma membrane) and thus the release of neurotransmitters. Each presynaptic terminal contains between 200 and 500 vesicles, though only a small proportion of these are ready to be released at any time. Vesicles in the presynaptic terminal move through a specific release cycle, including vesicle storage, priming for release, release, vesicle reformation, and reloading with neurotransmitter.
Factors that alter the presynapse resulting in either modification of the calcium channel conductance or modification of the vesicle cycle will yield changes in synaptic strength. One such factor is the cyclic nucleotide cAMP. An increase in cAMP presynaptically can enhance transmitter release by activating protein kinase A (PKA). PKA activation induces a decrease in a specific potassium channel conductance called a delayed rectifier current. Decreased delayed rectifier conductance will increase the calcium entry into the presynaptic terminal by increasing the duration of the action potential. In addition, a rise in cAMP can activate vesicular release from presynaptic terminals that were previously dormant. Such terminals are present, but do not release neurotransmitters in response to an action potential prior to a rise in cAMP. A morphologically distinct synapse that is physiologically dormant has been termed a silent synapse and can be the result of deficient presynaptic release, or a deficiency of transmitter receptors expressed postsynaptically.

The postsynaptic terminal can also be modified to produce changes in synaptic efficacy. Signaling molecules in the postsynaptic compartment such as protein kinase A (PKA) and the alpha subunit of calcium/calmodulin-dependent kinase II (α-CaMKII) are thought to play major roles in synaptic plasticity. For example, when a mouse is genetically altered to express a version of α-CaMKII incapable of activation, LTP and learning are disrupted. While α-CaMKII can directly phosphorylate neurotransmitter receptors leading to an increase in conductance, it is likely to play additional roles in synaptic plasticity as well. Neurotransmitter receptors can cycle in and out of the postsynaptic membrane (in a process not unlike the presynaptic vesicles), and α-CaMKII phosphorylation of an as yet unidentified substrate could lead to the rapid insertion of more receptors. This would result in LTP of an active synapse and the unsilencing of a synapse that was not previously expressing these receptors in its membrane. As stated above, there is substantial evidence implicating long-lasting changes in synaptic strength with the formation of memory. It should be noted that synapses do not act in isolation. The neural circuits to which they belong are a result of the many thousands of synapses contained therein. Although the cellular coding of information may be encoded at synapses, memory itself is likely dependent upon the circuit(s) in which they are contained.

Plasticity, memory, and aging

As humans age, an impairment of memory occurs that is not associated with neurological damage or disease. The age of onset for this decline varies, but it is clear that this is a selective deficit and not a generalized decrease in cognitive skills. Moreover, the deficit is also apparent in animal models of aging and is manifest as a greater number of trials required to memorize a task and a decrease in memory retention that begins approximately twenty-four hours post-training. Interestingly, LTP also changes with age, typically requiring a more robust stimulus to induce and yielding a synaptic potentiation that decays more rapidly. Since aging animals and humans both maintain the ability to store memory, the fundamental mechanisms that underlie information storage may remain essentially intact. The deficit may not be a lack of ability, but rather a decline in the efficiency of storageor an inability to maintain the neural plasticity induced during learning. Since the formation of memory is dependent on new protein synthesis, one way to address the decreased stability of memory is to identify proteins made during learning. Consistent with this, synaptic plasticity has at least two temporally distinct components: transient changes that do not require new protein synthesis, and enduring modifications (e.g., LTP and LTD) that require the production of new proteins. Identification of newly formed proteins, their site of action, and the molecular basis for their role in neural plasticity may provide insights into the maintenance of memory, and thus indicate clinical targets for the amelioration of age-related memory decline.
David G. Wells
See also Brain; Learning; Memory; Neurochemistry; Neurodegenative Diseases.

BIBLIOGRAPHY

Bliss, T. V. P., and Lomo, T. "Long-Lasting Potentiation of Synaptic Transmission in the Dentate Area of the Anaesthetized Rabbit Following Stimulation of the Perforant Path." Journal of Physiology (London) 232 (1973): 331356.
Cowen, W. M., and Kandel, E. R. "A Brief History of Synapses and Synaptic Transmission." In Synapses. Edited by W. M. Cowen, T. C. Sudhof and C. F. Stevens, Baltimore, Md.: The Johns Hopkins University Press, 2001. Pages 188.
Davis, H. P., and Squire, L. R. "Protein Synthesis and Memory: A Review." Psychology Bulletin 96 (1984): 518559.
Dudek, S. M., and Bear, M. F. "Homosynaptic Long-Term Depression in Area CA1 of Hipocampus and Effects of N-methyl-D-aspartate Receptor Blockade." Proceedings of the National Academy of Science 89 (1992): 43634367.
Foster, T. C. "Involvement of Hippocampal Synaptic Plasticity in Age-Related Memory Decline." Brain Research Review 30 (1999): 236249.
Giese, K. P.; Fedorov, N. B.; Filipkowski, R. K.; and Silva, A. J. "Autophosphorylation at Thr286 of the Alpha Calcium-Calmodulin Kinase II in LTP and Learning." Science 279 (1998): 870873.
Hayashi, Y.; Shi, S.-H.; Esteban, J. A.; Piccini, A.; Poncer, J. C.; and Malinow, R. "Driving AMPA Receptors into Synapses by LTP and CaMKII: Requirements for GluR1 and PDZ Domain Interactions." Science 287 (2000): 22622267.
Ma, L.; Zablow, L.; Kandel, E. R.; and Siegelbaum, S. A. "Cyclic AMP Induces Functional Presynaptic Boutons in Hippocampal CA3-CA1 Neuronal Cultures." National Neuroscience 2 (1999): 2430.
Tong, G.; Malenka, R. C.; and Nicoll, R. A. "Long-Term Potentiation in Cultures of Single Hippocampal Granule Cells: A Presynaptic Form of Plasticity." Neuron 16 (1996): 11471157.



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Neural plasticity: consequences of stress and actions of antidepressant treatment

Abstract

Neural plasticity is emerging as a fundamental and critical mechanism of neuronal function, which allows the brain to receive information and make the appropriate adaptive responses to subsequent related stimuli. Elucidation of the molecular and cellular mechanisms underlying neural plasticity is a major goal of neuroscience research, and significant advances have been made in recent years. These mechanisms include regulation of signal transduction and gene expression, and also structural alterations of neuronal spines and processes, and even the birth of new neurons in the adult brain. Altered plasticity could thereby contribute to psychiatric and neurological disorders. This article revievi/s the literature demonstrating altered plasticity in response to stress, and evidence that chronic antidepressant treatment can reverse or block the effects, and even induce neural piasiicity-iike responses. Continued elucidation of the mechanisms underlying neural plasticity will lead to novel drug targets that could prove to be effective and rapidly acting therapeutic interventions.
Keywords: signal transduction, gene expression, neurotrophic factor, neurogenesis, neuronal atrophy
Neural plasticity is a fundamental process that allows the brain to receive information and form appropriate adaptive responses to the same or similar stimuli. The molecular and cellular adaptations underlying learning and memory are the best-characterized and moststudied examples of neural plasticity. However, many different stimuli can activate neural plasticity processes in different brain structures, including environmental, social, behavioral, and pharmacological stimuli. In fact, it could be argued that neural plasticity is one of the most essential and important processes that the brain performs as it relates to many types of central nervous system functions.
Thus, disrupted or abnormal plasticity could lead to maladaptive neuronal responses and abnormal behavior. This could occur in response to genetic abnormalities of the cellular machinery required for plasticity, and abnormal or inappropriate stimuli. For example, exposure to inappropriate or prolonged stress has been reported to alter molecular and cellular markers of neural plasticity, and could contribute to stress-related mood disorders. This review will discuss the literature demonstrating altered neural plasticity in response to stress, and clinical evidence indicating that altered plasticity occurs in depressed patients. The second part of the review will present evidence that antidepressant treatment blocks the effects of stress or produces plasticity -like responses.

General mechanisms of neural plasticity

Neural plasticity encompasses many different types of molecular and cellular responses that occur when cells in the brain are induced to respond to inputs from other cells or circulating factors. The systems that have been most extensively studied are cellular and behavioral models of learning and memory, including long-term potentiation (LTP), in slices of brain and rodent models of behavior. The mechanisms identified for learning and memory most likely also subserve plasticity occurring in other regions and for other adaptive functions of the brain. This section will briefly discuss some general mechanisms and concepts of plasticity.

Mechanisms of acute neural plasticity: synaptic transmission and protein kinases

The effects underlying the rapid responses to neuronal activation are mediated by activation of the excitatory neurotransmitter glutamate and regulation of intracellular signaling cascades (for a review of acute mechanisms underlying LTP, see reference 1). Glutamate causes neuronal depolarization via activation of postsynaptic ionotropic receptors that increase intracellular Na+. This leads to the subsequent activation of /V-mcthyl-D-aspartatc (NMDA) receptors and the resulting influx of Ca2+. Ca2+ is a major intracellular signaling molecule that activates a signaling cascade, including activation of Ca2+/ calmodulin-dependent protein kinase. Within minutes to hours, activation of glutamate and Ca2+-dependent pathways can result in structural alterations at the level of dendritic spines. Spines mark the location of glutamate synapses and have been the subject of intensive investigation for understanding synaptic plasticity.2 Changes in the shape and even number of spines can occur very rapidly (minutes to hours) after glutamate stimulation. These alterations are made permanent or long-term when they arc stabilized or consolidated, a process that requires gene expression and protein synthesis.

Mechanisms of long-term plasticity: gene expression and protein synthesis

The Ca2+/cyclic adenosine monophosphate (cAMP) response element (CaRE) binding protein (CREB) is one of the major transcription factors that mediate the actions of Ca2+, as well as cAMP signaling. CREB has been reported to play a role in both cellular and behavioral models of learning and memory.3 There are a number of gene targets that are influenced by Ca2+, cAMP, and CREB, and the pattern of gene regulation is dependent on the cell type, the length of stimulation, as well as the magnitude of stimulation. Gene targets that have been implicated in learning and memory, and are relevant to the effects of stress and antidepressant treatment, are the neurotrophic factors. Of particular interest is brain-derived neurotrophic factor (BDNF), one of the most abundant neurotrophic factors in the brain.

Altered neural plasticity in response to stress

Recent reports have demonstrated altered molecular and cellular responses to stress and have contributed to the hypothesis that altered neural plasticity contributes to stress-related psychiatric illnesses. Some examples of stress responses are discussed in this section.

Stress alters learning and memory

Stress is known to significantly influence learning and memory, and the effects are dependent on the type, duration, and intensity of the stressor. Emotional arousal can enhance learning and memory via synaptic plasticity of amygdala-dependent pathways, and this is thought to be the basis for intense, long-term memories of traumatic events and posttraumatic stress disorder.4,5 However, stress can also impair subsequent learning and memory and can even lead to amnesia.6 The influence of stress on hippocampal-dependent learning is complex and dependent on the type of learning task.
In studies of LTP, a consistent suppression of neural plasticity is observed after exposure to stress or adrenal glucocorticoids.6,7 In one of these studies, the suppression of LTP was observed after exposure to an uncontrollable stressor and correlated with behavioral performance in a learning and memory task. Giving the animals control over the stress (ie, the stress could be terminated) did not lead to reduced LTP or decreased learning and memory.8 A role for BDNF in the actions of stress on LTP has also been suggested.9 For additional references and discussion of the effects of stress on learning and memory, see the reviews in references 4 to 7.

Stress causes atrophy of hippocainpal neurons

One of the best-characterized examples of altered structural plasticity in response to stress is the atrophy of hippocampal neurons, which was first described by McEwen and colleagues (Figure 1.).10 They found that repeated restraint stress results in atrophy of the dendrites of CA3 pyramidal neurons in the hippocampus, measured as a decrease in the number and length of apical dendrites.11 The reduction in dendritic arborization was found to be dependent on long-term, repeated exposure to restraint stress (3 weeks) and to be reversible when the animals are removed from stress. The atrophy of CA3 pyramidal cells appears to result from the elevation of adrenal glucocorticoids that occurs during stress because chronic administration of corticosteronc, the active form in rodent, results in a similar decrease in number and length of dendrites.12 The actions of stress and glucocorticoids are blocked by administration of an NMDA receptor antagonist, indicating that this glutamate receptor is required for atrophy of CA3 neurons.10 Atrophy of CA3 pyramidal neurons occurs after 2 to 3 weeks of exposure to restraint stress or more long-term social stress, and has been observed in rodents and tree shrews.11-13 In contrast to the atrophy of hippocampus, recent studies demonstrate that chronic stress causes hypertrophy of neurons in the amygdala.14 This study found chronic immobilization stress increased the dendritic arborization of pyramidal neurons in the basolateral amygdala, but decreased dendrite length and branching in the CA3 pyramidal neurons of the hippocampus. Hypertrophy of the amygdala could underlie increased learning and memory as a result of stressinduced emotional arousal, and may be relevant to the pathophysiology of stress-related disorders, including anxiety, posttraumatic stress, and depression. Increased arborization of neurons in the amygdala could thereby enhance emotional states or disrupt normal processing of emotional responses.
Figure 1.
Model of hippocampal plasticity showing structural alterations in response to stress: atropy of CA3 pyramidal neurons and decreased neurogenesis of dentate gyrus granule cells. Stress results in powerful effects on the hippocampus, partly because of the ...

Stress decreases neurogenesis in the adult hippocampus

In addition to regulation of the morphology of neurons in the hippocampus, stress influences the number of newborn neurons or neurogenesis in the adult hippocampus15,16 (Figures 1 and 2.) The hippocampus is one of two brain regions where neurogenesis continues to occur in adult organism (the other region is in the subventricular zone). In the hippocampus, neural progenitor cells are found in the subgranular zone, between the granule cell layer and the hilus. These cells give rise to newborn cells that migrate into the granule cell layer and mature into neurons with the morphological and physiological characteristics of adult granule cells.17 Interestingly, the process of neurogenesis is highly regulated by a variety of stimuli and can be considered a form of neural plasticity. For example, enriched environment, exercise, and learning increase neurogenesis, while aging and exposure to drugs of abuse decrease neurogenesis.15,16,18
Figure 2.
Model demonstrating the regulation of adult neurogenesis in the hippocampus. Neural progenitor cells are restricted to the subgranular zone (SGZ) that is located between the granule cell layer (GCL) and hilus. These progenitor cells give rise to newborn ...
In addition to these factors, stress also results in a dramatic downrcgulation of neurogenesis in the hippocampus.10,18 Exposure to just a single stressor is sufficient to significantly decrease neurogenesis in the adult hippocampus. Adult neurogenesis is decreased by different types of stress, including subordination stress,19 predator odor,20 maternal separation,21 and footshock.22 In addition, exposure to inescapable stress in the learned helplessness model of depression decreases adult neurogenesis and this effect correlates with behavioral despair in this model.22 Moreover, the reduction in neurogenesis and the behavioral despair is reversed by antidepressant treatment.

Regulation of CREB and decreased expression of BDNF in response to stress

Stress results in a wide range of effects that influence many different neurotransmitter and neuropeptide systems, signal transduction pathways, and altered gene expression. The hallmark of the stress response is activation of the hypothalamic-pituitary-adrcnal (HPA) axis, which includes increased circulating levels of adrenal glucocorticoids. The hippocampus contains veryhigh levels of glucocorticoid receptors and is therefore significantly impacted by stress. As mentioned above, studies by McEwen and colleagues have demonstrated that glucocorticoids contribute to the atrophy and decreased neurogenesis of hippocampal neurons resulting from exposure to stress.10
In addition, stress is reported to influence CREB and BDNF in the hippocampus and other brain regions. The transcriptional activity of CREB is regulated by phosphorylation and levels of phospho-CREB are used as an indirect measure of CREB activation and function (Figure 3.) The, regulation of phospho-CREB is complex and is dependent on the brain region and whether the stress is acute or chronic.23-26 Acute stress increases levels of phospho-CREB in many limbic regions associated with mood disorders and this may represent a normal or appropriate adaptive responsiveness.24 In contrast, chronic stress leads to decreased levels of phosphoCREB in many limbic brain regions, which could lead to decreased plasticity and function.26
Figure 3.
Model demonstrating the upregulation of the cyclic adenosine monophosphate (cAMP)-cAMP response element binding protein (CREB) cascade and expression of brain-derived neurotrophic factor (BDNF) by antidepressant treatment. Chronic, but not acute, antidepressant ...
Stress has profound effects on the expression of BDNF in the hippocampus. Levels of BDNF expression in hippocampus are dramatically downregulated by both acute and chronic stress, and this effect could contribute to the atrophy and decreased neurogenesis caused by stress (Figure l).27-29 The role of other factors that could underlie the actions of stress on adult neurogenesis is a subject of interest and could lead to novel targets for drug development.

Atrophy of limbic brain structures in depressed patients

Evidence from basic research studies provide strong support for the hypothesis that stress-related illnesses such as depression could include alterations in brain structure and neural plasticity. Indeed, direct evidence to support this hypothesis has been provided by brain imaging and postmortem studies of depressed patients.

Evidence from brain imaging studies

Magnetic resonance imaging studies have demonstrated that the size of certain brain structures is decreased in mood disorder patients. In particular, these studies demonstrate that the volume of the hippocampus is decreased in patients with depression.30,31 Reduced hip pocampal volume is also observed in patients with posttraumatic stress disorder (PTSD).32 The reduction in hippocampal volume is directly related to the length of illness.33,34 In addition to hippocampus, atrophy of prefrontal cortex and amygdala - brain regions that control cognition, mood, and anxiety - has also been reported in patients with depression or bipolar disorder.35

Evidence from postmortem studies

Atrophy of hippocampus or other brain regions could result from loss of cells (neurons or glia) or decreased size of the cell body or neuronal processes. The most extensive studies have been conducted on prefrontal and cingulatc cortex and demonstrate that the neuronal body size and number of glia is decreased in depressed patients.36-38 There is much less known about the hippocampus and additional studies will be required to determine what accounts for the atrophy of hippocampus observed in depressed patients.
Postmortem analysis of CREB and BDNF has also provided evidence consistent with a loss of neural plasticity in depression. Levels of CREB arc decreased in the cerebral cortex of depressed patients or suicide victims.39,40 Levels of BDNF are also decreased in prefrontal cortex and hippocampus of depressed patients.41 Reduced levels of CREB and BDNF“, two molecular markers of neural plasticity, indicate that the ability of limbic brain structures to mount adaptive responses is compromised in depressed patients.

Antidepressant treatment increases neural plasticity

In contrast to the effects of stress, antidepressant treatment results in molecular and cellular responses that demonstrate an increase in neural plasticity. Moreover, these studies have paved the way for additional studies that demonstrate that antidepressant treatment results in structural remodeling. In many cases, the effects of antidepressant treatment oppose or reverse the effects of stress. Taken together, these findings provide additional support for the hypothesis that neural plasticity plays a significant role in the treatment, as well as the pathophysiology of mood disorders. The evidence for regulation of neural plasticity at the level of neurogenesis, signal transduction, and gene expression is discussed in the second half of this review.

Antidepressant treatment increases adult neurogenesis

Neurogenesis is increased by chronic antidepressant administration

One of the most surprising discoveries of recent times in the field of depression is that antidepressant treatment regulates neurogenesis in the adult hippocampus (Figures 1 and 2). In contrast to the actions of stress, chronic antidepressant treatment increases the number of newborn neurons in the adult hippocampus of rodents or tree shrews.42,43 The upregulation of neurogenesis is dependent on chronic antidepressant treatment, consistent with the time course for the therapeutic action of antidepressants.43 In addition, different classes of antidepressants, including serotonin (5-hydroxytryptamine [5-HT]) and noradrenaline reuptake inhibitors, and electroconvulsive seizures are reported to increase adult neurogenesis.43-45 Antidepressant treatment influences two important aspects of neurogenesis, the rate of cell proliferation (ie, the number of newborn neurons) and the survival of newborn neurons.46 An increase in the number of newborn neurons could contribute to the reversal of hippocampal atrophy observed in depressed patients.

Antidepressant treatment blocks the downregulation of neurogenesis caused by stress

The influence of antidepressant treatment in the context of stress has also been examined. These studies demonstrate that chronic antidepressant treatment can block or reverse the downregulation of neurogenesis that results from exposure to stress. Several different types of stress have been tested, including blockade of intruder stress,42 maternal separation,47 and learned helplessness.22 In addition, different types of antidepressants have been tested, including an atypical antidepressant, tianeptine,42 a selective serotonin reuptake inhibitor (SSRI),22,47 and a neurokinin-1 receptor antagonist.48.
The influence of antidepressant treatment on the atrophy of CA3 pyramidal neurons resulting from chronic exposure to stress has been examined. These studies demonstrate that chronic administration of tianeptine blocks the atrophy of CA3 apical dendrites that is caused by stress.12 Chronic administration of an SSRI antidepressant did not block the atrophy of CA3 neurons in this study Analysis of dendrite branch number and length is tedious and labor intensive, but additional studies of other antidepressants are necessary to determine the relevance of this effect in the actions of antidepressant treatment.

A functional role for neurogenesis in the action of antidepressant treatment

A major issue in the field of adult neurogenesis is how to test the function of newborn neurons. A recent study has addressed this question by using a combination of irradiation and mutant mouse approaches.49 This study demonstrates that focused irradiation of hippocampus in the mouse completely blocks neurogenesis and there was a corresponding blockade of the behavioral actions of antidepressant treatment in two behavioral models, novelty suppressed feeding and chronic mild stress. In addition, Santarelli et al49 studied the effects of antidepressants in mice with a null mutation of the 5-HT1A receptor, a subtype that has been implicated in the actions of antidepressant treatment. They found that upregulation of neurogenesis by chronic administration of an SSRI was completely blocked in 5-HT1A null mutant mice, and that the behavioral effects of SSRI treatment were similarly blocked. These results are the first evidence that increased neurogenesis is necessary for an antidepressant response in behavioral models. rFh ere arc a few limitations to this study. First, although novelty-suppressed feeding is responsive to chronic antidepressant treatment - and this is why it was chosen - this paradigm is a better model of anxiety than depression. Second, although the effects of antidepressant treatment were blocked, irradiation and 5-HT1A null mutation alone, in the absence of antidepressant administration, did not produce a depressive phenotype. This is consistent with another report demonstrating that decreased neurogenesis is not correlated with behavior in the learned helplessness model of depression.50 Together these studies indicate that neurogenesis is not required for baseline response. However, it is possible that intact neurons are sufficient to sustain baseline response and that more long-term inhibition of neurogenesis would be required to influence activity.

The cAMP-CREB cascade and depression

Neural plasticity upon antidepressant treatment is likely to involve adaptations of multiple intracellular signaling cascades and even interactions of these pathways. One of the pathways that is regulated by antidepressant treatment and has been demonstrated to contribute to the actions of chronic antidepressant responses is the cAMP-CREB cascade, the subject of this section. However, it is likely that other signaling pathways are also regulated by - and play a role in - the actions of antidepressants. For reviews covering other signal transduction pathways, see reference 51 and 52.

Antidepressant treatment upregulates the cAMP CREB cascade

Several studies have investigated the influence of antidepressant treatment on the cAM'P-CREB pathway (Figure 3).53,54 This work demonstrates that chronic antidepressant treatment upregulates the cAMP second-messenger cascade at several different levels. This includes increased coupling of the stimulatory G protein to adenylyl cyclase, increased levels of cAMP-dependent protein kinase (PKA), and increased levels of CREB as well as phospho-CREB.55-57 Upregulation of these components of the cAMP-CREB signaling pathway is dependent, on chronic antidepressant treatment, consistent with the time course for the therapeutic action of antidepressants. In addition, upregulation of the cAMP-CREB cascade is observed in response to chronic administration of different classes of antidepressants, indicating that this is a common target of antidepressant treatment.
In addition to phosphorylation by PKA, CREB is also phosphorylated by Ca2+-dependent kinases, such as Ca2+/calmodulin-dependent protein kinase, and by mitogen-activated protein kinase pathways (Figure 3). In this way, CREB can serve as a target for multiple signal transduction pathways and neurotransmitter receptors that activate these cascades.

Activation of the cAMP-CREB cascade produces an antidepressant response

Direct, evidence for cAMP-CREB signaling in the action of antidepressant treatment has been tested by pharmacological, viral vector, and mutant mouse approaches. First, drugs that block the breakdown of cAMP produce an antidepressant response in behavioral models of depression.54 The primary target for inhibition of cAMP breakdown is cAMP-specific phosphodiesterase type IV (PDE4), and rolipram was one of the first selective PDE4 inhibitors. In addition, we have found that chronic rolipram administration increases neurogenesis in adult hippocampus.46,58
Second, viral expression of CREB in the hippocampus of rat produces an antidepressant response in the forced swim and learned helplessness models of depression.59 However, further studies demonstrated that the effects of CREB are dependent on the brain region where it is expressed. For example, expression of CREB in the nucleus accumbens produces a prodepressant effect, while expression of a dominant, negative mutant of CREB results in an antidepressant response in the forced swim test.60 Transgenic expression of dominant negative CREB in the nucleus accumbens is consistent with this effect.61 The different behavioral effects of CREB can be explained by different target genes in the hippocampus (ic, BDNF) versus the nucleus accumbens (ie,prodynorphin).

Regulation of neurotrophic factors and depression

The regulation of CREB by antidepressant treatment indicates that regulation of gene expression also plays a role in the actions of antidepressants. There have been many gene targets identified for antidepressants,51,52 but BDNF is one that has gained attention and is relevant to neural plasticity responses to antidepressant medications. Studies to identify additional gene targets and gene profiles using gene microarray analysis are currently being conducted.

Antidepressant treatment upregulates BDNF

Neurotrophic factors were originally identified and studied for their role in development, and neuronal survival. However, it is now clear that these factors are expressed in the adult brain, arc dynamically regulated by neuronal activity, and are critical for the survival and function of adult neurons. On the basis of these considerations, it is clear why decreased expression of BDNF could have serious consequences for the function of limbic brain structures that control mood and cognition. In contrast, antidepressant treatment results in significant upregulation of BDNF in the hippocampus and cerebral cortex of rodents.28,53,54 Increased expression of BDNF is dependent on chronic treatment, and is observed with different classes of antidepressants, but not other psychotropic drugs. The induction of BDNF would be expected to protect neurons from damage resulting from stress, elevated glucocorticoids, or other types of neuronal insult.

BDNF has antidepressant effects in behavioral models of depression

The possibility that BDNF contributes to the actions of antidepressant treatment is supported by behavioral studies of recombinant BDNF and transgenic mouse models. Microinfusions of BDNF into the hippocampus produce an antidepressant-like response in the learned helplessness and forced swim models of depression.62 The antidepressant, effect of BDNF is observed after a single infusion, compared with repeated administration of a. chemical antidepressant, and is relatively long-lasting (up to 10 days after infusion). Transgenic overexpression of a dominant negative mutant of the BDNF receptor, trkB, in the hippocampus and other forebrain structures is also reported to block the effect, of antidepressant treatment, demonstrating that BDNF signaling is necessary for an antidepressant response.63
Microinfusions of BDNF into the dorsal raphe, a midbrain region where 5-HT cell bodies are localized, also produces an antidepressant response in the learned helplessness model.64 Together, these studies indicate that BDNF could contribute to antidepressant responses in both forebrain and brain stem structures by affecting different populations of neurons. Alternatively, it is possible that, microinfusions of BDNF into the hippocampus influence 5-HT neuronal function by acting at presynaptic sites, and could therefore enhance 5-HT signaling as observed after brain stem infusions of BDNF.64

A neurotrophic hypothesis of depression

Basic research and clinical studies of BDNF have resulted in a. neurotrophic hypothesis of depression and antidepressant action.53,54 This hypothesis is based in part. on studies demonstrating that stress decreases BDNF, reduces neurogenesis, and causes atrophy or CA3 pyramidal neurons. Brain imaging and postmortem studies provide additional support, demonstrating atrophy and cell loss of limbic structures, including the hippocampus, prefrontal cortex, and amygdala. In contrast, antidepressant treatment, opposes these effects of stress and depression, increasing levels of BDNF, increasing neurogenesis, and reversing or blocking the atrophy and cell loss caused by stress and depression. Additional brain imaging and postmortem studies, as well as basic research approaches will be required to further test this hypothesis. In any case, the studies to date provide compelling evidence that, neural plasticity is a. critical factor in the pathophysiology and treatment of depression.

Antidepressants influence other neurotrophic factor systems

Because of the preclinical and clinical evidence implicating neurotrophic factors in the pathophysiology and treatment of depression, studies have been conducted to examine other neurotrophic factor systems. One of the most robust effects identified to date is that antidepressant treatment increases the expression of fibroblast. growth factor-2 (FGF-2).65 FGF-2 is known to have a potent influence on neurogenesis during development and in the adult brain, and could contribute to antide pressant regulation of neurogenesis. Studies are under way to examine the role of FGF-2 in antidepressant regulation of neurogenesis and regulation of behavior in models of depression. Several other growth factors have been identified by microarray analysis and gene expression profiling, including vascular endothelial growth factor, neuritin, and VGF.66 Studies are currently under way to determine the functional significance of these growth factors in models of depression.

Clinical evidence of relevance of neural plasticity to antidepressant treatment

Basic research studies clearly demonstrate that antidepressant treatment regulates signal transduction, gene expression, and the cellular responses that, represent neural plasticity. This issue is more difficult, to address in clinical studies, but evidence is slowly accumulating. Brain imaging studies have been conducted to examine the influence of antidepressants on the volume of limbic brain regions. One study demonstrates that hippocampal atrophy is inversely proportional to the length of time a patient receives antidepressant medication.67 A longitudinal study of PTSD patients before and after antidepressant treatment has found that there is a. partial reversal of hippocampal atrophy in patients receiving medication.68 The latter study demonstrated a corresponding increase in verbal declarative memory in response to antidepressant treatment.
Evidence at the molecular level is also provided by postmortem studies. Levels of CREB immunoreactivity are increased in patients receiving antidepressant treatment at the time of death relative to unmedicated patients.39 In addition, levels of BDNF are increased in patients taking an antidepressant at the time of death.59 Although these effects must be replicated and extended (for example, to the regulation of neurogenesis) in additional banks of postmortem tissue, the results are consistent with the hypothesis that neural plasticity is upregulatcd in patients receiving antidepressant medication.

Novel targets for the treatment of depression

The hypothesis that antidepressant treatment increases neural plasticity provides a number of novel targets for drug development. However, as with any fundamentally important mechanism, care must be taken that the drugs developed for such targets do not interfere with the normal function of the brain. Nevertheless, regulation of neural plasticity is an exciting area of research for design of new drugs for a variety of indications, including learning, memory, cognition, mood, and neurodegenerative disorders. This section discusses a few of these targets in the context of the pathways regulated by antidepressants and stress.

Targets for antidepressant regulation of neurogenesis

Identification of the signal transduction and gene expression pathways that are responsible for the actions of antidepressant regulation of neurogenesis is a subject, of intense investigation. Activation of the cAMP-CREB signaling cascade using either pharmacological or transgenic approaches is reported to increase both proliferation and survival of newborn neurons in the hippocampus,46,58 supporting the possibility that antidepressants increase neurogenesis via regulation of this intracellular pathway. Gene targets of CREB, as well as other neurotrophic/growfh factors that, have been shown to regulate adult neurogenesis, include BDNF, FGF-2, and insulin-like growth factor-1 , to name but. a few.18 Because antidepressant treatment increases the expression of both BDNF and FGF-2, these two factors are currently being investigated. This is just a partial listing of the signal transduction cascades and factors that could contribute to antidepressant regulation of adult neurogenesis.

Targets for regulation of the cAMP-CREB cascade

There are several different sites within the cAMP pathway that could be targeted for drug development. One that has already proven to be effective for antidepressant treatment is blockade of PDE4 and the breakdown of cAMP. Rolipram is a PDF'4-selective inhibitor that has been demonstrated to have antidepressant efficacy in early clinical trials and behavioral models of depression.69,70 However, the clinical use of rolipram has been limited by its side effects, primarily nausea.
The identification of four different. PDE4 isozymes that are equally inhibited by rolipram raises the possibility that one of the isozymes underlies the antidepressant actions of rolipram, while another mediates its side effects. Studies are currently under way to characterize the regional distribution and function of the three PDE4 isozymes expressed in brain (PDE4A, PDE4B, and PDE4D) and the role of these isozymes in the actions of antidepressant treatment.71 Studies of mutant mice demonstrate that null mutation of PDE4D produces an antidcpressant-like phenotype indicating a role for this isozyme,72 and similar studies are currently under way for PDE4A and PDE4B.

BDNF as a target for drug development

The use of BDNF and other neurotrophic factors for the treatment of neurological disorders has been a subject of interest, for several years, although problems with delivery, efficacy, and side effects have hampered these efforts. To more directly replicate the in vivo situation, it may be possible to stimulate the expression of endogenous BDNF expression by stimulating signaling pathways known to regulate this neurotrophic factor. First, activation of the cAMP-CREB cascade by inhibition of PDE4 increases the expression of BDNF.56
Small molecular agonists for neurotransmitter receptors have also exhibited some promise. Activation of ionotropic glutamate receptors increases BDNF expression and could be targeted for the treatment of depression.73 One drug that modulates glutamate transmission and increases BDNF expression is memantine.74 Riluzole, a. sodium channel blocker, also increases BDNF expression, as well as neurogenesis in adult hippocampus.75 Specific 5-HT and norepinephrine receptor subtypes that activate cAMP (eg, β-adrenergic, 5-HT7), Ca2+, or mitogen-activated protein kinase (α1-adrenergic, 5-HT1A) pathways could also be targets for development. Characterization of the antidepressant actions of these compounds will be needed, as well as identification of additional neurotransmitter and signal transduction systems that regulate BDNF

Conclusions

Studies of the molecular and cellular mechanisms underlying neural plasticity responses in learning and memory, as well as fear, anxiety, depression, and drug abuse to name but a few, are some of the most exciting and rapidly advancing areas of research in neuroscience. Progress in our understanding of neural plasticity has profound implications for the treatment of a number of psychiatric and neurodegenerative disorders, and for enhancing performance in what are considered normal subjects. One of the promising aspects of neural plasticity is that it implies that the alterations that occur are reversible, even neuronal atrophy and cell loss. Reversibility of structural as well as functional plasticity has already been demonstrated in response to pharmacological treatments or even behavioral therapy. As the fundamental mechanisms of neural plasticity are further elucidated, new targets and paradigms for enhancing plasticity will be revealed and will lead to more effective and faster-acting therapeutic interventions.

Selected abbrewiations and acronyms

BDNFbrain-derived neurotrophic factor
cAMPcyclic adenosine monophosphate
CaREcAMP response element
CREBcAMP response element binding protein
FGF-2fibroblast growth factor-2
5-HT5 -hydroxy tryptamine (serotonin)
LTPlong-term potentiation
NMDAN-methyl-D-aspartate
PDE4phosphodiesterase type IV
PKAprotein kinase
SSRIselective serotonin reuptake inhibitor

Notes

This work is supported by USPHS grants MH45481 and 2 P01 MH25642, a Veterans Administration National Center Grant for posttraumatic stress disorder, and by the Connecticut Mental Health Center.

REFERENCES

1. Malenka R., Nicoll RA. Long-term potentiation - a decade of progress?. Science. 1999;285:1870–1874. [PubMed]
2. Lamprecht R., LeDoux J. Structural plasticity and memory. Nat Rev Neurosci. 2004;5:45–54. [PubMed]
3. Silva A., Kogan JH., Frankland PW., Kida S. CREB and memory. Ann Rev Neurosci. 1998;21:127–148. [PubMed]
4. Cahill L., McGaugh JL. Mechanisms of emotional arousal and lasting declarative memory. Trends Neurosci. 1998;21:294–299. [PubMed]
5. LeDoux J. Emotion circuits in the brain. Ann Rev Neurosci. 2000;23:155–184. [PubMed]
6. Kim J., Diamond DM. The stressed hippocampus, synaptic plasticity and lost memories. Nat Rev Neurosci. 2002;3:453–462. [PubMed]
7. Pavlides C., Nivon LG., McEwen BS. Effects of chronic stress on hippocampal long-term potentiation. Hippocampus. 2002;12:245–257. [PubMed]
8. Shors T., Seib TB., Levine S., Thompson RF. Inescapable versus escapable shock modulates long-term potentiation in the rat hippocampus. Science. 1989;244:224–226. [PubMed]
9. Zhou J., Zhang F., Zhang Y. Corticosterone inhibits generation of longterm potentiation in rat hippocampus slice: involvement of brain-derived neurotrophic factor. Brain Res. 2000;885:182–191. [PubMed]
10. McEwen B. Stress and hippocampal plasticity. Curr Opin Neurobiol. 1999;5:205–216. [PubMed]
11. Wooley CS., Gould E., McEwen BS. Exposure to excess glucocorticoids alters dendritic morphology of adult hippocampal pyramidal neurons. Brain Res. 1990;531:225–231. [PubMed]
12. Watanabe Y., Gould E., Daniels DC., Cameron H., McEwen BS. Tianeptine attenuates stress-induced morphological changes in the hippocampus. Eur J Pharmacol. 1992;222:157–162. [PubMed]
13. Margarinos A., McEwen BS., Flugge G., Fuchs E. Chronic psychosocial stress causes apical dendritic atrophy of hippocampal CA3 pyramidal neurons in subordinate tree shrews. J Neurosci. 1996;16:3534–3540. [PubMed]
14. Vyas A., Mitra R., Shankaranarayana Rao BS., Chattarji S. Chronic stress induces contrasting patterns of dendritic remodeling in hippocampal and amygdaloid neurons. J Neurosci. 2002;22:6810–6818. [PubMed]
15. Gage F. Mammalian neural stem cells. Science. 2000;287:1433–1438. [PubMed]
16. Gould E., Beylin A., Tanapat P., Reeves A., Shors TJ. Learning enhances adult neurogenesis in the hippocampal formation. Nat Neurosci. 1999;2:260–265. [PubMed]
17. van Praag H., Schlinder AF., Christie BR., Toni N., Palmer TD., Gage FH. Functional neurogenesis in the adult mouse dentate gyrus. Nature. 2002;415:1030–1034. [PubMed]
18. Duman R., Malberg J., Nakagawa S. Regulation of adult neurogenesis by psychotropic drugs and stress. J Pharmacol Exp Ther. 2001;299:401–407. [PubMed]
19. Gould E., McEwen BS., Tanapat P., Galea LAM., Fuchs E. Neurogenesis in the dentate gyrus of the adult tree shrew is regulated by psychosocial stress and NMDA receptor activation. J Neurosci. 1997;17:2492–2498. [PubMed]
20. Tanapat P., Hastings NB., Rydel TA., Galea LAM., Gould E. Exposure to fox odor inhibits cell proliferation in the hippocampus of adult rats via an adrenal hormone-dependent mechanism. J Cornp Neurol. 2001;437:496–504. [PubMed]
21. Lee K., Lynch KR., Nguyen T., et al. Cloning and charactization of additional members of the G protein-coupled receptor family. Biochim Biophys Acta. 2000;1490:311–323. [PubMed]
22. Malberg J., Duman RS. Cell proliferation in adult hippocmpus is decreased by inescapable stress: reversal by fluoxetine treatment. Neuropsychopharmacology. 2003;28:1562–1571. [PubMed]
23. Barrot M., Olivier JD., Perrotti LI., et al. CREB activity in the nucleus accumbens shell controls gating of behavioral responses to emotional stimuli. Proc Natl Acad Sci USA. 2002;99:11435–11440. [PMC free article] [PubMed]
24. Bilang-Bleuel A., Rech J., De Carli S., Holsboer F., Reul JMHM. Forced swimming evokes a biphasic response in CREB phosphorylation in extrahypothalamic limbic and neocortical brain structures in the rat. Eur J Neurosci. 2002;15:1048–1060. [PubMed]
25. Bruijnzeel A., Stam R., Compaan JC., Wiegant VM. Stress-induced sensitization of CRH-ir but not P-CREB-ir responsivity in the rat central nervous system. Brain Res. 2001;908:187–196. [PubMed]
26. Trentani A., Kuipers SD., Ter Horst GJ., Den Boer JA. Selective chronic stress-induced in vivo ERK1/2 hyperphosphorylation in medial prefrontocortical dendrites: implications for stress-related cortical pathology?. Eur] Neurosci. 2002;15:1681–1691. [PubMed]
27. Duman R. Role of neurotrophic factors in the etiology and treatment of mood disorders. Neuromol Med. 2004;5:11–26. [PubMed]
28. Nibuya M., Morinobu S., Duman RS. Regulation of BDNF and trkB mRNA in rat brain by chronic electroconvulsive seizure and antidepressant drug treatments. J Neurosci. 1995;15:7539–7547. [PubMed]
29. Smith MA., Makino S., Kvetnansky R., Post RM. Stress alters the express of brain-derived neurotrophic factor and neurotrophin-3 mRNAs in the hippocampus. J Neurosci. 1995;15:1768–1777. [PubMed]
30. Bremner J., Narayan M., Anderson ER., Staib LH., Miller H., Charney DS. Smaller hippocampal volume in major depression. Am J Psychiatry. 2000;157:115–117. [PubMed]
31. Sheline Y., Wany P., Gado MH., Csernansky JG., Vannier MW. Hippocampal atrophy in recurrent major depression. Proc Natl Acad Sci USA. 1996;93:3908–3913. [PMC free article] [PubMed]
32. Bremner JD., Randall P., Scott TM., et al. MRI-based measurement of hippocampal volume in patients with combat-related posttraumatic stress disorder. Am J Psychiatry. 1995;152:973–981 . [PMC free article] [PubMed]
33. MacQueen G., Campbell S., McEwen BS., et al. Course of illness, hippocampal function, and hippocampal volume in major depression. Proc Natl Acad Sci USA. 2003;100:1387–1392. [PMC free article] [PubMed]
34. Sheline Y., Sanghavi M., Mintun MA., Gado MH. Depression duration but not age predicts hippocampal volume loss in medically healthy wormen with recurrent major depression. J Neurosci. 1999;19:5034–5043. [PubMed]
35. Manji H., Duman RS. Impairments of neuroplasticity and cellular resilience in severe mood disorders: implications for the development of novel therapeutics. Psychopharmacol Bull. 2001;35:5–49. [PubMed]
36. Cotter D., Mackay D., Landau S., Kerwin R., Everall I. Reduced glial cell density and neuronal size in the anterior cingulate cortex in major depressive disorder. Arch Gen Psychiatry. 2001;58:545–553. [PubMed]
37. Ongur D., Drevets WC., Price JL. Glial reduction in the subgenual prefrontal cortex in mood disorders. Proc Natl Acad Sci U S A. 1998;95:13290–13295. [PMC free article] [PubMed]
38. Rajkowska G., Miguel-Hidalgo JJ., Wei J., et al. Morphometric evidence for neuronal and glial prefrontal cell pathology in major depression. Biol Psychiatry. 1999;45:1085–1098. [PubMed]
39. Dowlatshahi D., MacQueen GM., Wang JF., Young LT. Increased temporal cortex CREB concentrations and antidepressant treatment in major depression. Lancet. 1998;352:1754–1755. [PubMed]
40. Dwivedi Y., Rizavi HS., Conley RR., Tamminga CA., Pandey GN. Altered gene expression of brain-derived neurotrophic factor and receptor tyrosine kinase B in postmortem brain of suicide subjects. Arch Gen Psychiatry. 2003;60:804–815. [PubMed]
41. Dwivedi Y., Rizavi HS., Roberts RC., Conley RC., Tamminga CA., Pandey GN. Reduced activation and expression of ERK1/2 MAP kinase in the postmortem brain of depressed suicide subjects. J Neurochem. 2001;77:916–928. [PubMed]
42. Czeh B., Michaelis T., Watanabe T., et al. Stress-induced changes in cerebral metabolites, hippocampal volume, and cell proliferation are prevented by antidepressant treatment with tianeptine. Proc Natl Acad Sci USA. 2001;98:12796–12801. [PMC free article] [PubMed]
43. Malberg J., Eisch AJ., Nestler EJ., Duman RS. Chronic antidepressant treatment increases neurogenesis in adult hippocampus. J Neurosci. 2000;20:9104–9110. [PubMed]
44. Madsen T., Treschow A., Bengzon J., Bolwig TG., Lindvall O., Tingstrôm A. Increased neurogenesis in a model of electroconvulsive therapy. Biol Psychiatry. 2000;47:1043–1049. [PubMed]
45. Manev H., Uz T., Smalheiser NR., Manev R. Antidepressants alter cell proliferation in the adult brain in vivo and in neural cultures in vitro. Eur J Pharmacol. 2001;411:67–70. [PubMed]
46. Nakagawa S., Kim JE., Lee R., et al. Regulation of neurogenesis in adult mouse hippocampus by cAMP and cAMP response element-binding protein. J Neurosci. 2002;22:9868–9876. [PubMed]
47. Lee H., Kim JW., Yim SV., et al. Fluoxetine enhances cell proliferation and prevents apoptosis in dentate gyrus of maternally separated rats. Mot Psychiatry. 2001;6:725–728. [PubMed]
48. van der Hart M., Czeh B., de Biurrun G., et al. Substance P receptor antagonist and clomipramine prevent stress-induced alterations in cerebral metabolites, cytogenesis in the dentate gyrus and hippocampal volume. Mol Psychiatry. 2002;7:933–941. [PubMed]
49. Santarelli L., Saxe M., Gross C., et al. Requirement of hippocampal neurogenesis for the behavioral effects of antidepressants. Science. 2003;301:805–809. [PubMed]
50. Vollmayr B., Simonis C., Weber S., Gass P., Henn F. Reduced cell proliferation in the dentate gyrus is not correlated with the development of learned helplessness. Biol Psychiatry. 2003;54:1035–1040. [PubMed]
51. Manji H., Drevets WC., Charney DS. The cellular neurobiology of depression. Nat Med. 2001;7:541–547. [PubMed]
52. Nestler E., Barrot M., DiLeone RJ., Eisch AJ., Gold SJ. Monteggia LM. Neurobiology of depression. Neuron. 2002;34:13–25. [PubMed]
53. Duman R., Heninger GR., Nestler EJ. A molecular and cellular theory of depression. Arch Gen Psychiatry. 1997;54:597–606. [PubMed]
54. Duman R., Malberg J., Nakagawa S. C D'Sa. Neuronal plasticity and survival in mood disorders. Biol Psychiatry. 2000;48:732–739. [PubMed]
55. Nestler E., Terwilliger RZ., Duman RS. Chronic antidepressant administration alters the subcellular distribution of cAMP-dependent protein kinase in rat frontal cortex. J Neurochem. 1989;53:1644–1647. [PubMed]
56. Nibuya M., Nestler EJ., Duman RS. Chronic antidepressant administration increases the expression of cAMP response element binding protein (CREB) in rat hippocampus. J Neurosci. 1996;16:2365–2372. [PubMed]
57. Thome J., Sakai N., Shin KH., et al. cAMP response element-mediated gene transcription is upregulated by chronic antidepressant treatment. J Neurosci. 2000;20:4030–4036. [PubMed]
58. Nakagawa S., Kim JE., Lee R., Chen J., Fujioka T., Malberg J. Localization of phosphorylated cAMP response element-binding protein in immature neurons of adult hippocampus. J Neurosci. 2002;22:9868–9876. [PubMed]
59. Chen A-H., Shirayama Y., Shin KH., Neve RL., Duman RS. Expression of the cAMP response element binding protein (CREB) in hippocampus produces antidepressant effect. Biol Psychiatry. 2001;49:753–762. [PubMed]
60. Pliakas A., Carlson RR., Neve RL., Konradi C., Nestler EJ., Carlezon WA. Altered responsiveness to cocaine and increased immobility in the forced swim test associated with elevated CREB expression in the nucleus accumbens. J Neurosci. 2001;21:7397–7403. [PMC free article] [PubMed]
61. Newton S., Thome J., Wallace TL., et al. Inhibition of cAMP response element-binding protein or dynorphin in the nucleus accumbens produces an antidepressant-like effect. J Neurosci. 2002;24:10883–10890. [PubMed]
62. Shirayama Y., Chen AC., Nakagawa S., Russell RS., Duman RS. Brain-derived neurotrophic factor produces antidepressant effects in behavioral models of depression. J Neurosci. 2002;22:3251–3261. [PubMed]
63. Saarelainen T., Hendolin P., Lucas G., et al. Activation of the trkB neurotrophin receptor is induced by antidepressant drugs and is required for antidepressant-induced behavioral. effects. J Neurosci. 2003;23:349–357. [PubMed]
64. Siuciak JA., Lewis DR., Wiegand SJ., Lindsay R. Antidepressant-like effect of brain-derived neurotrophic factor (BDNF). Pharmacol Biochem Behav. 1997;56:131–137. [PubMed]
65. Mallei A., Shi B., Mocchetti I. Antidepressant treatments induce the expression of basic fibroblast growth factor in cortical and hippocampal neurons. 2002;61:1017–1024. [PubMed]
66. Newton S., Collier E., Hunsberger J., Adams D., Salvanayagam E., Duman RS. Gene profile of electroconvulsive seizures: induction of neurogenic and angiogenic factors. J Neurosci. 2003;23:10841–10851. [PubMed]
67. Sheline Y., Gado MH., Kraemer HC. Untreated depression and hippocampal volume loss. Am J Psychiatry. 2003;160:1–3. [PubMed]
68. Vermetten E., Vythilingam M., Southwick SM., Charney DS., Bremner JD. Long-term treatment with paroxetine increases verbal declarative memory and hippocampal volume in posttraumatic stress disorder. Biol Psychiatry. 2003;54:693–702. [PMC free article] [PubMed]
69. Horowski R., Sastre-Y-Hernandez M. Clinical effects of the neurotrophic selective cAMP phosphodiesterase inhibitor rolipram in depressed patients: global evaluation of the preliminary reports. CurrTher Res. 1985;38:23–29.
70. Wachtel H. Potential antidepressant activity of rolipram and other selective cyclic adenosine 3',5“-monophosphate phosphodiesterase inhibitors. Neuropharmacology. 1983;22:267–272. [PubMed]
71. Takahashi M., Terwilliger R., Lane S., Mezes PS., Conti M., Duman RS. Chronic antidepressant administration increases the expression of cAMP phosphodiesterase 4A and 4B isoforms. J Neurosci. 1999;19:610–618. [PubMed]
72. Zhang H-T., Huang Y., Jin SJC., et al. Antidepressant-like profile and reduced sensitivity to rolipram in mice deficient in the PDE4D phosphodiesterase enzyme. Neuropsychopharmacology . 2002;27:587–595. [PubMed]
73. Li X., Tizzano JP., Griffey K., Clay M., Lindstron T., Skolnick P. Antidepressant-like actions of an AMPA receptor potentiator (LY392098). Neuropharmacology. 2001;40:1028–1033. [PubMed]
74. Marvanova M., Lakso M., Pirhonen J., Nawa H., Wong G., Castren E. The neuroprotective agent memantine induces brain-derived neurotrophic factor and trkB receptor expression in rat brain. Mol Cell Neurosci. 2001;18:247–258. [PubMed]
75. Katoh-Semba R., Asano T., Ueda H., et al. Riluzole enhances expression of brain-derived neurotrophic factor with consequent proliferation of granule precursor cells in the rat hippocampus. FASEBJ. 2001;16:1328–1330. [PubMed]

To all Black women from all Black men by Eldridge Cleaver

Queen-Mother-Daughter of Africa
Sister of My Soul
Black Bride of My Passion
My Eternal Love

Kathleen and Eldridge Cleaver


I greet you, my Queen, not in the obsequious whine of a cringing Slave to which you have become accustomed, neither do I greet you in the new voice, the unctuous supplications of the sleek Black Bourgeoisie, nor the bullying bellow of the rude Free Slave---but in my own voice do I greet you, the voice of the Black Man.

And although I greet you anew, my greeting is not new, but as old as the Sun, Moon, and Stars. And rather than mark a new beginning, my greetings signifies only my Return.

I have returned from the dead. I speak to you in the Here And Now. I was dead for four hundred years. For four hundred years you have been a woman alone, bereft of her man, a manless woman. For four hundred years I was neither your man nor my own man. The white man stood between us, over us, around us. The white man was your man and my man. Do not pass lightly over this truth, my Queen, for even the fact of it has burned into the marrow of our bones and diluted our Blood, we must bring it to the surface of the mind, into the realm of knowing, glue our gaze upon it and stare at it as at a coiled serpent in a baby's playpen or the fresh flowers on a mother's grave. It is to be pondered and realized in the heart, for the heel of the white man's boot is our point of departure, our point of Resolve and Return---the bloodstained pivot of our future. (but I would ask you to recall, that before we could come up from slavery, we had to be pulled down from our throne.)

Across the naked abyss of negated masculinity, of four hundred years minus my Balls, we face each other today, My Queen. I feel a deep, terrifying hurt, the pain of humiliation of the vanquished warrior. The shame of the fleet-footed sprinter who stumbles at the start of the race. I feel unjustified. I can't bear to look into your eyes. Don't you know (surely you must have noticed by now : four hundred years ) that for four hundred years I have been unable to look squarely into your eyes? I tremble inside each time you look at me. I can feel . . . in the ray of your eye, from a deep hiding place, a long-kept secret you harbor.

That is the unadorned truth. Not that I would have felt justified, under the circumstances, in taking such liberties with you, but I want you to know that I feared to look into your eyes because I knew I would find reflected there a merciless Indictment of my impotence and a compelling challenge to redeem my conquered manhood.

My Queen, it is hard for me to tell you what is in my heart for you today---what is in the heart of all my black brothers for you and all your black sisters---and I fear I will fail unless you reach out to me, tune in on me with the antenna of your love, the sacred love in the ultimate degree which you were unable to give to me because I, being dead, was unworthy to receive it; that perfect, radical love of black on which our Fathers thrived. Let me drink from the river of your love as its source, let the lines of force of your love seize my soul by its core and heal the wound of my Castration, let my convex exile end its haunted odyssey in your concave essence which receives that it may give. Flower of Africa, it is only through the liberating power of your re-love that my manhood can be redeemed. For it is in your eyes, before you, that my need is to be justified, Only, only, only you and only you can condemn or set me free.

Be convinced , sable sister, that the past is no forbidden vista upon which we dare not look, out of a phantom fear of being, as the wife of Lot, turned into pillars of salt. Rather the past is an omniscient mirror: we gaze and see reflected there ourselves and each other---what we used to be, what we are today, how we got this way, and what we are becoming. To decline to look into the Mirror of Then, my heart, is to refuse to view the face of Now.


I have died the ninth death of the cat, have seen Satan face to face and turned my back on God, have dined in the Swine's Trough, and descended to the uttermost echelon of the pit, have entered the Den and seized my Balls from the teeth of a roaring lion

Black Beauty, in impotent silence I listened, as if to a symphony of sorrows, to your screams for help, anguished pleas of terror that echo still throughout the Universe and through the mind, a million scattered screams across the painful years that merged into a single sound of pain to haunt and bleed the soul, a white-hot sound to char the brain and blow the fuse of thought, a sound of fangs and teeth sharp to eat the heart, a sound of moving fire, a sound of frozen heat, a sound of licking flames, a fiery-fiery sound, a sound of fire to burn the steel out of my Balls, a sound of Blue fire, a Bluesy sound, the sound of dying, the sound of my woman in pain, the sound of my woman's pain, THE SOUND OF MY WOMAN CALLING ME, ME, I HEARD HER CALL FOR HELP, I HEARD THAT MOURNFUL SOUND BUT HUNG MY HEAD AND FAILED TO HEED IT, I HEARD MY WOMAN'S CRY, I HEARD MY WOMAN'S SCREAM, I HEARD MY WOMAN BEG THE BEAST FOR MERCY, I HEARD HER BEG FOR ME, I HEARD MY WOMAN BEG THE BEAST FOR MERCY FOR ME, I HEARD MY WOMAN DIE, I HEARD THE SOUND OF HER DEATH AS SHE SCREAMED FOR ME TO COME TO HER AS SHE LAY IN THE CLUTCHES OF THE BEAST, I CAN STILL HEAR HER, I CAN STILL HEAR HER, THE SOUND OF YOUR SCREAMS THAT ECHO WITHIN ME, A SNAPPING SOUND, A BREAKING SOUND, A SOUND THAT SOUNDED FINAL, THE LAST SOUND, THE ULTIMATE SOUND, THE SOUND OF DEATH, ME, I HEARD, I HEAR IT EVERY DAY, I HEAR HER NOW . . .

I HEAR YOU NOW . . . I HEAR YOU. . . .I heard you then . . . your scream came like a searing bolt of lighting that blazed a white streak down my black back. In a cowardly stupor, with a palpitating heart and quivering knees, I watched the Slaver's lash of death slash through the opposing air and bite with teeth of fire into your delicate flesh, the black and tender flesh of Afrikan Motherhood, forcing the startled Life untimely from your torn and outraged womb that incubated Ethiopia and populated Nubia and gave forth Pharaohs unto Egypt, the womb that painted the Congo black and motherland Zulu, the womb of Mero, the womb of Ghana, the womb that felt the might of Chaka before he saw the Sun, the Holy Womb, the womb that knew the future form of Mzee Jomo Kenyatta, the womb of Mau Mau, the womb of the blacks, the womb that nurtured Toussaint L'Ouverture, that warmed Nat Turner, and Gabriel Prosser, and Denmark Vesey, the black womb that surrendered up in tears that nameless and endless chain of Africa's Cream, the Black Cream of the Earth, that nameless and endless black chain they sank in heavy groans into oblivion in the great abyss, the womb that received and nourished and held firm the seed and gave back Sojourner Truth, and Sister Tubman, and Rosa Parks, and Bird, and Richard Wright, and your other works of art who wore and wear such names as Marcus Garvey and DuBois and Kwame Nkrumah and Paul Robeson and Malcolm X and Robert Williams, and the one you bore in pain and called Elijah Muhammad, but most of all that nameless one they tore out of your womb in a flood of murdered Blood that splashed upon and seeped into the mud. And Patrice Lumumba, and Emmett Till, and Mack Parker.

O, My Soul I become a sniveling craven, a funky punk, a vile, groveling bootlicker, with my will to oppose petrified by a cosmic fear of the Slavemaster. Instead of inciting the Slaves to rebellion with eloquent oratory, I soothed their hurt and eloquently sang the Blues Instead of hurling my life with contempt into the face of my Tormentor, I shed your precious blood When Nat Turner sought to free me for my Fear, my Fear delivered him up unto the butcher ---a martyred monument to my Emasculation. My spirit was unwilling and my flesh was weak.

Ah, eternal ignominy I, the Black Eunuch, divested of my Balls, walked the earth with my mind locked in Cold Storage. I would kill a black man or woman quicker than I'd smash a fly, while for the white man I would pick a thousand pounds of cotton a day. What profit is there in the blind, frenzied efforts of the (Guilty) Black Eunuchs (Justifies ) who hide their wounds and scorn the truth to mitigate their culpability through the pallid sophistry of postulating a Universal Democracy of Cowards, pointing out that in history no one can hide, that if not at one time then surely at another the iron heel of the Conqueror has ground into the mud the Balls of Everyman? Memories of yesterday will not assuage the torrents of blood that flow today from my crotch. Yes, History could pass for a scarlet text, its jot and title graven red in human blood. More armies than shown in the books have planted flags on foreign soil leaving Castration in their wake. But no Slave should die a natural death. There is a point where Caution ends and Cowardice begins. Give me a bullet through the brain from the gun of the beleaguered oppressor on the night of siege. Why is there dancing and singing in the Slave Quarters? A Slave who dies of natural causes cannot balance two dead flies in the Scales of Eternity. Such a one deserves rather to be pitied than mourned.

Black woman, without asking how, just say that we survived our forced march and travail through the Valley of Slavery, Suffering, and Death---there, that Valley beneath us hidden by that drifting mist. Ah, what sights and sounds and pain lie beneath that mist And we had thought that our hard climb out of that cruel valley led to some cool, greem and peaceful, sunlit place---but it's all jungle here, a wild and savage wilderness that's overrun with ruins.

But put on your crown, my Queen, and we will build a New City on these ruins.

Black Bird Press News & Review: Police Terror in America: Notes from Beyonce', Kev Choice, June Jordan, Marvin X, Fritz Pointer, Fahizah Alim, Dominique Villanueva

Black Bird Press News & Review: Police Terror in America: Notes from Beyonce', Kev Choice, June Jordan, Marvin X, Fritz Pointer, Fahizah Alim, Dominique Villanueva

Marvin X notes on discussion of Black Hollywood unChained at SF Main Library

Bay Area authors rock San Francisco Main Library discussion of Black Hollywood unChained anthology

Ancestor Austin C. Clarke, giant of Canadian African literature 
On his way to the San Francisco Library, Marvin X was elated when he checked his mail and found a kind note from Nikki Giovanni, thanking him for informing her Austin joined the ancestors. 


 Left to Right: Justin Desmangles, Jesse Allen-Taylor, Dr. Halifu Osumare, Marvin X, Ishmael Reed
photo Johnnie Burrell

Preface

In Black Hollywood Unchained, Ishmael Reed gathers an impressive group of scholars, critics, intellectuals, and artists to examine and respond to the contemporary portrayals of Blacks in films. Using the 2012 release of the film Django Unchained as the focal point of much of the discussion, these essays and reviews provide a critical perspective on the challenges facing filmmakers and actors when confronted with issues on race and the historical portrayal of African American characters. Reed also addresses the black community's perceptiveness as discerning and responsible consumers of film, theatre, art, and music.
--Justin Mesmangles



On Sunday, July 3, contributing writers to the anthology Black Hollywood unChained, held a spirited discussion on the collection of essays edited by Ishmael Reed, Third World Press, Chicago. The discussion was facilitated by Justin Desmangles who questioned Ishmael Reed, Jesse Allen-Taylor,
Dr. Halifiu Osumare and Marvin X. It  was  sponsored by Before the Columbus Foundation and the African American Center of the San Francisco Public Library, and videoed for later broadcast by Johnnie Burrell of International Media TV.Com. It will air on July 9 and available on Youtube.

Justin Desmangles, Chair of Before Columbus Foundation, journalist, poet, posed questions to the authors based on their essays. We must await the video for an accurate narration of the event but one question was why must Hollywood continues writing our stories that they can only tell from the white supremacy mythological viewpoint. Jews would not let Nazis write their history, although it was noted Jews take the liberty to narrate North American African history or the white version of it that is nothing less than pure fantasy or stories from the white world of make believe. Jesse Allen-Tayor said Black actors are essentially whores who are pimped by producers and are so desperate for roles they will perform anything, no matter how demeaning and despicable.

Dr. Halifu Osumare explained when the book project began, it was focused on the film Django but evolved into a general discussion on the condition of Blacks in Hollywood. Halifu noted how director Tarantino used the Yoruba myth of Oshun to depict the Black woman as goddess, although she wasn't sure the director had knowledge of Yoruba mythology. She also appreciated how the woman was freed by her man and road to freedom on her own horse to show a certain level of independence yet in harmony with her man.

Marvin X said the story of an individual Black man saving his woman is noble but insufficient because we need stories of communal liberation rather than individual. Referring to his essay, Justin asked Marvin X about the traumatic slave syndrome of the oppressed as described in modern times by Dr. Frantz Fanon. Marvin X said, firstly, Elder Ed Howard, a founding member of Oakland's Afro-American Association, has called for us not to use the term slaves but rather say we were/are Africans caught in the American Slave System. Marvin X said we are still suffering from the traumatic stress of the American slave system. Upon emancipation, we had no therapy and still have none. Justin noted how the nine people were killed in the North Charleston church, South Carolina and what this says about how religion is used to pacify us to the degree we immediately ask forgiveness and mercy for the killer. Marvin replied that their mentality shows the degree of addiction to white supremacy religion. The Southern Blacks still live in fear, Marvin said. For example, when he finished writing How to Recover from the Addiction to White Supremacy in Beaufort, South California and went to Staples for copies, the clerk asked where he was from? He told the Black sister, I'm from here, but she said no you're not. When he asked why she doubted him, she replied because we don't say White Supremacy down here, we know it but don't say it. This reveals a pervasive level of fear disguised as manners.

Jesse-Allen-Taylor would have none of putting down of the South. He's lived in South Carolina and is the author of a novel on South Carolina, Sugarie Rising, and he noted a unique town north of Charleston that had no Confederate statues and that there were people still resisting white supremacy.

Marvin said one of his last book tours through South Carolina his hosts told him to shut up and don't say nothing while you're here, and furthermore, we are not going to give you a book party or help you promote your book, just enjoy yourself and go on up the road. Marvin said he did as his hosts ordered which gave him time to visit the African Village in Sheldon, South Carolina. He noted the young Yoruba King's father was from Harlem and helped spread Yoruba culture throughout the United States. Halifu Osumare agreed the Yoruba King in South Carolina is highly respected, including a visit from the Oba of Ife, Nigeria. It was asked why don't more writers utilize African mythology in their work. Marvin recalled that in the play A Black Mass, Amiri Baraka utilized myths from Islam (the myth of Yakub) and Yoruba mythology. Baraka had studied the Yoruba religion as did many  poets and writers during the Black Arts Movement. The founding  Oba of Olatunji Village married Amiri and Amina Baraka.

Justin probed for more religious influences in North American African culture. Panelists replied the Catholic church has made ample use of Yoruba and Vudun in their services and even the Protestant religious community employ the Holy Ghost ritual similar to riding the god. Ishmael Reed noted how many writers have researched and studied Yoruba and Vudun myth-rituals in our culture, especially Katharyn Dunham. During the Q and A, videographer Ken Johnson stated he wished we would explain more of this mythology because he'd never heard of Yemanja or Oshun and would like to know.

Ishmael, whom we graciously acknowledge as one of our Master writers or griots ,who has overwhelming knowledge  of European and African mythology, yet he admitted ignorance of African revolts against the slave system.  Marvin told Ishmael and the audience to check out the History Channels documentary Slave Catchers and Resisters, also Negro Slave Revolts by Herbert Aptheker.

Jesse Allen-Taylor said the truth is that there was almost daily resistance to the American Slave System. When  the Roots and  Neo-Roots films series came into the discussion, Halifu said  the original Roots had the positive because for the first time many Blacks and Whites got some understanding of the American Holocaust, and this was a good thing. Marvin X replied, I don't want to see no more films about slavery, only resistance. "Show me Toussaint, Garbriel Prosser, Nat Turner, Denmark Vessey. If I go to one more movie about slavery, I might kill some white people." He quoted Amiri Baraka's Dutchman, in which the character Clay says, "If Bessie Smith had killed some white people, she wouldn't have needed to sing the Blues,  she could have talked very straignt and plain about the world."

Ishmael Reed was asked about his review of the Broadway musical Hamilton. Ishmael said it was a scam, pure and simple. He said his research revealed Hamilton was a slave owner, not an abolitionist  as the original text claimed. Hamilton had slaves and so did his wife. Thus Hamilton is a thousand dollar ticket scam and a reverse of the Black Arts Movement revolution. Hamilton put Black and minority actors in the costumes of the Slave Masters and it ain't even Halloween.  Ishmael noted in his review that at least during the Black Arts Movement of the 60s, writers took the language of the master and flipped it, but in Hamilton they took the Hip Hop poetry and rap and put it in the mouth of the slave masters!


Ishmael mentioned that Malcolm X was less than truthful when he claimed it was in Mecca that he discovered blue-eyed devil Muslims who exercised true Islamic brotherhood. He noted Malcolm had met blue-eyed Muslims in New York at the United Nations, so his letter from Mecca is a sham and Marvin X agreed. As per Islamic brotherhood, Marvin X interjected, "My friends, including members of the Last Poets, made their pilgrimage to Mecca forced to ride in the back of the bus from Amman, Jordan to Mecca, Saudi Arabia,  forced by white racist Turkish Muslims who were then made to pay a fee for disrespecting the Black Muslims from America. And just as 11AM Sunday morning is the most segregated hour in Christian American, 1PM Friday is the most segregated hour in Muslim America.
--Marvin X

Left to Right: Justin Desmangles, Jesse Allen-Taylor, Dr. Halifu Osumare, Marvin X, Ishmael Reed
photo Johnnie Burrell

Thursday, July 7, 2016

Police Terror in America: Notes from Beyonce', Kev Choice, June Jordan, Marvin X, Fritz Pointer, Fahizah Alim, Dominique Villanueva


























From the archives: Marvin X on the assassination of Chauncey Bailey and the Cross and Lynching Tree

Chauncey Bailey, Editor, Oakland Post Newspaper, slain in broad daylight, downtown Oakland, 14th and Alice, BAMBD district

The Cross and the Lynching Tree

From the 12th floor office of the Oakland Post newspaper at 14th and Franklin, one can look down the block to a tree at 14th and Alice. Chauncey Bailey was lynched near that tree, although it was not in the tradition of a white lynching, but in the neo-America, his lynchers were black. And although the suspect is a young black man, there are witnesses who say the killer was an older person. Does it really matter, except for the fact that we are now doing the work of the KKK. We wear the hoods these days, and the fad is to wear gear with “stupid” designs, including skull and bones, thus signaling to the world our deathly intentions. We have become death angels, as sinister as the suicide bombers in the Middle East, although we have no purpose, no mission, except to kill another black, for of the nearly 130 killed in Oakland last year, not one white man was killed by a black. And for the most part, this is true throughout America. Our youth exhibit an animal consciousness as opposed to their spiritual consciousness. No, they do not use the mind God gave them, as my mother told me to do, but they seem motivated by a demonic spirit of hatred of self and kind, causing them to perpetuate the internal violence Dr. Franz Fanon wrote about in Wretched of the Earth.

Bay Area artists/activists celebrate the life of Chauncey Bailey at the Joyce Gordon Gallery, Oakland
photo Gene Hazzard/Adam Turner

Mao Zedong told us some deaths are higher than Mount Tai, some deaths lighter than a feather. At least Chauncey gave his life for the cause of truth, no matter that we did not always agree with his abrasive attitude, who can deny the man was dedicated to seeking the truth? We all have defects of character, but are we fulfilling our life’s mission as Chauncey was doing? Are we trying to inform the blind, deaf and dumb, to educate the ignorant? Many of us say let the blind stay blind, and that the youth are a lost cause, yet we saw in the film the Great Debaters, youth will do the right things when guided right by sincere and dedicated adults. The only excuse for youth behavior is adult behavior!

The tree at 14th and Alice stands still, a monument to a fallen soldier. From the window, our eyes zoom down to the tree, eyes full of tears and heart full of sorrow. Bill Moyers asked Rev. James Cone the meaning of the cross and the lynching tree. He said they are one and the same, for on the cross Jesus was crucified and on the tree the black man was done the same. And just as Jesus transcended the cross, the black man must rise above his self crucifixion and ascend to spiritual consciousness. The crucifixion ends when the resurrection and ascension begins. We must rise up from the grave of ignorance, from the lynching tree of hatred, jealousy and envy. We must heal from the wretchedness that allows us to kill another brother at the drop of a hat, yet never approach the real enemy. And perhaps the real enemy doesn’t exist except inside of our selves. White supremacy/lunacy has no power over us except when we allow it. As Rev. Cone explained, the lynching tree has no power over us because in our crucifixion comes resurrection and ascension.

Paul Cobb observed how white women can jog pass West Oakland’s Campbell Village housing projects at night without fear. No one dare harm them because they are white and thus sacred. To speak harshly to them is a terrorist threat, to harm them is a hate crime that qualifies for the death penalty. But there is no crime for speaking harshly to another black, and killing another black does not qualify as a hate crime, although most surely it is the absolute essence of hate, self hate.

And so we dig our own grave these days. We put the noose around our necks, as some rappers have demonstrated. We killed our brother Chauncey because he was just another nigguh, therefore worthless, in the imagination of the killers, whoever they are. And then perhaps they recognized his importance and were instructed to eliminate him, for writers and journalists are killed around the world, simply for their dedication to telling the truth.
But we see after the thousands and thousands of words written about him, we see death has no sting, it has no victory.

On a horrible day last August, the tree at 14th and Alice gave forth a strange fruit that shall rise from the earth and give blessings from high heaven. Because Chauncey lived, we shall be a better people, a people who shall one day fulfill our radical tradition and destiny to free ourselves and the world. The attempt was made with the Oakland branch of the Pullman Porters, and it was made with the Black Panthers. Chauncey extended that tradition into the present era, for he gave his life in the cause of truth, freedom, justice and equality. Yes, he transcended the lynching tree. His death was not lighter than a feather but higher than Mount Tai.
--Marvin X
Marvin X
photo by Spencer Wilkerson, Alice Street film project

The Cross and the Lynching Tree (James Hal Cone and Bill Moyers)

We live under the shadow of death! If you ain't Jesus, why do you get crucified like Jesus?

Under the Shadow of Death

By The Most Honorable Elijah Muhammad 



We, the Black lost-found of our people here in America live under the shadow of death by way of cowardly enemies. Every one of us—the cowardly enemies seek our deaths, one way or another.
police_beating.jpg
The cowardly enemies will not fight you as a brave man would fight you if they think that you would fight back. They will steal on you when you least expect an attack from them. 


We live under the shadow of death. We fled from the cowardly enemy devils of the South, seeking refuge in the same cowardly enemies’ brother in the North. The enemy devils of the South followed us to the North to see that his brother of the North does not treat us any better than they did in the South.

They seek police jobs so that they can beat and kill us who are trying to escape. They seek to kill us, or get us killed, at any price. They do not care about our loyalty to them. In their hearts there is death for us, the Black Man in America.
Today, they hold out promises to you only to deceive you. They know that Allah (God) is here offering to seat us in heaven at once. And since hell is their appointed place, they are trying to get us to go to hell with them on false promises. I have told you. Believe it or let it alone. We live "Under The Shadow of Death."



Wednesday, July 6, 2016

Flim: Alice Street, a BAMBD related project

Culture Spy



  The Alice Street mural.
The Alice Street mural.

Thursday, June 16, 2016

Forthcoming Documentary Fights Cultural Erasure in Oakland

This week, the trailer and crowdfunding campaign was released for 'Alice Street,' a movie about a mural and much more.

By Arielle Swedback

East Bay Express 


Earlier this week, the Community Rejuvenation Project (CRP), a local arts nonprofit, released a trailer and crowdfunding campaign for its anticipated documentary, Alice Street. The film recounts the genesis of a mural that has thrust public art into the forefront of its neighborhood’s gentrification debate.

Nestled at the crossroads of Oakland’s Chinatown district and the Afro-diasporic community based at the adjacent Malonga Casquelourd Center for the Performing Arts, the CRP mural aimed to capture the neighborhood’s historic intersectionality. The art, which celebrates artists and folk traditions from both cultural enclaves, has been hailed as a beacon of resilience in the face of heightening community displacement due to gentrification.

Oakland muralists Pancho Peskador and Desi Mundo were commissioned in 2010 to paint the three blighted walls surrounding a parking lot at 1401 Alice Street. The artists filmed extensive interviews with both Chinese-American and Black residents to understand their respective communities’ histories of out-group discrimination and personal experiences of cultural perseverance.

These oral histories, along with twenty-five days of time-lapse videography showing the mural’s installation and footage of the Malonga Center community meetings and performances that fostered the mural’s conception, were the nascent vision of director Spencer Wilkinson’s documentary.

But then the tangible reality of Oakland’s gentrification problem presented itself — directly in front of the Alice Street mural.

As the Express has previously reported, only three-months after the mural's completion, CRP leaders learned of plans to develop a 126-unit condominium complex in a privately-owned parking lot in front of the artwork. The mural, which cost $80,000 in grant money from the City of Oakland and community crowdfunding, would be entirely obscured.

The film follows the community polemic launched in response to the development and the wider dialogue surrounding housing inequity in the region. The Alice Street mural has become a chief symbol of cultural resilience in a neighborhood that is being threatened by Oakland’s displacement crisis.

Alice Street is scheduled to premiere in October 2016. But the filmmakers are currently fundraising the cost of post-production in order to complete it. They aim to raise $12,000, the first $8,000 of which will be matched by the East Bay Community Foundation. Contribute to the Generosity page here or watch the trailer below.


Website: www.alicestreetfilm.com

Marvin X appears in Alice Street film
photo by Spencer Wilkerson, Alice Street film project producer



Alice Street


Dallas Sniper's sister called pigs murderers in Facebook post night before brother's killing spree

Johnson and her brother are seen in Facebook photo.





The night before Micah X. Johnson ambushed police in Dallas, his younger sister posted a Facebook message deriding white cops as murderers and declaring that, “I for one think these cops need to get a taste of the life we now fear.”

As seen above, Nicole Johnson’s post noted that, “White ppl have and will continue to kill us off.”
Shortly before Johnson posted her message Wednesday evening, she uploaded a New York Times video that included footage of the struggle that ended Tuesday night with the death of Alton Sterling, who was shot to death by Baton Rouge cops.

In a caption accompanying the video, Johnson wrote, “Makes me so mad.” She then asked, “When we decide we had enough n fight back.”

Earlier this afternoon, Johnson wrote that she was “shutting down my Facebook as the news is stealing my private words, photos and harassing my friends. When its safe i will hop back on here.” Her page, however, remains online.