Institute of the Black World Defends Black Lives Matter

Press Release Contact: Don Rojas Email: donjbrojas@gmail.com     Institute of the Black World Defends Black Lives Matter Calls on Pres. Obama to Visit Baton Rouge and St. Paul, as Well as Dallas   New York, July 10, 2016...The Institute of the Black World 21st Century (IBW) is defending the Black Lives Matter Movement against false criticism from right-wing political pundits that the Movement was responsible for the tragic deaths of five Dallas police officers.   While condemning the murders, by callous policemen and by a disturbed former Afghanistan veteran, IBW is also calling on President Obama to be "fair and balanced" in his posture towards the horrific and terrorist-like murders in recent days by visiting Baton Rouge and St. Paul after he has visited Dallas on Tuesday and to demonstrate, in both words and deeds, his equal concern for the families and communities of those who died in all three cities.   In citing the official statement put out by Black Lives Matter (BLM) leaders on Friday, IBW said the unvarnished truth is that the Black Lives Matter Movement has never called for the murder of police officers and has said over and over again that it is time in this country for policing to be accountable, transparent and responsible.   "We agree with the BLM that this is what communities in the United States want to see from the people who protect and serve them," said IBW's President Dr. Ron Daniels. "There needs to be accountable, responsive, transparent policing that has oversight from those communities and that is accountable to the communities they are supposed to protect and serve. We also call on civil rights and human rights organizations to stand with the Black Lives Matter Movement to ensure that they are not scapegoated, repressed and marginalized."   Daniels called for an urgent national conversation on race and structural racism saying such a conversation must involve all strata of society and should be more than "just talk and pious rhetoric" and, instead, must produce a public policy agenda of action items that include thorough-going criminal justice reform, comprehensive community-based economic development, and a reparations program that seeks social justice and a starts a process of repairing and healing the ongoing devastating social and psychological consequences from the historical crimes of chattel slavery and legal Jim Crow segregation.   "America needs to find the honesty and moral courage to confront the sins of its past and the living consequences of those sins today," said Daniels. "Now is the time for all people of good will to commit themselves to this imperative."   The IBW President also noted that the time is long overdue to end the War on Drugs which over the past 25 years has contributed to a spike in police brutality, accompanied by an explosion in the mass incarceration of young black and brown men in vastly disproportionate numbers across the country. "The War on Drugs has been a war on black and brown communities which has broken thousands of families and beat a path of social and economic devastation across the United States," said Daniels.   The events in the USA in recent days have sparked outrage and concern in black communities across the world, manifested in a huge demonstration in support of the Black Lives Matter Movement this weekend in London, another in Canada, and expressions of horror in radio and television call-in programs across the Caribbean and in the government of the Bahamas issuing a travel advisory urging its citizens visiting the USA to exercise "extreme caution around police."   **************

Police: from Problem to Solution--The Newark, New Jersey Model

Newark, NJ Mayor Ras Baraka and Marvin X


When I was in Newark, New Jersey for the last rites of my friend and comrade, poet/activist Amiri Baraka, his son Ras then a city councilman but was running for mayor. He told me then, "Marvin we got Black brothers on the police force with legal guns who back us, i.e., the community." And I observed positive police/community relations. It is a different feeling when you know the police are on your side. As a matter of fact, during the time of the funeral the police were in and out of the Baraka's house socializing with and protecting Newark's "first family".  Police blocked off the block where the Baraka family lives in the hood.

I was informed some of the officers had grown up with the Baraka children or their parents had been part of the Newark black consciousness, cultural and political movement that was critical in the election of Newark's first Black mayor, Kenneth Gibson. In short, the police were an integral part of the community, as opposed to an occupying army.

Now let's be clear, Ras informed me there were police who supported the opposition, but he felt confident with the percentage of officers on his (the peoples) side. Ironically, I was at the Baraka house once on AB's  birthday (October 7) when the opposition sent officers with warrants to arrest his sons for failure to pay child support. This was done by his political enemies to rattle his cage on his birthday. They do play hard ball in Newark and the opposition is serious. There are former Newark mayors who went down in disgrace for their negrocities (AB term, not mine, he wanted me to let you know) but have sons that they want to be mayor.

Of course Ras won the election as mayor, guided by his brother Amiri, Jr.'s (Middy) strategic planning. Their mother, Mrs. Amina Baraka, has kept me informed of her son's progress as mayor. Even the New York Times gave him brownie points for his first 100 days in office.

Mrs. Baraka informed me there have been no police killings since Ras became Mayor, although brothers killing brothers has not stopped. Mayor Baraka has police walking through the hood, Black and White officers, smiling and greeting the people. Mrs. Baraka said she doesn't know, and many people don't know, what to think of the white officers smiling so much.

But clearly, community policing is working, thus Newark can be and should be a  model for cities trying to upgrade their police departments from acting like brute beasts in blue uniforms. Why should police take the life of the mostly poor, mentally ill and drug addicted? Why would you kill a man hustling single cigarettes, DVDs and CDs? Why would you kill a man for a broken tail light or failure to signal a lane change.? Why should a man suffer a broken spine from a ride in the paddy wagon?

Surely after all the hell the Black Panther Party suffered trying to combat police terror and brutality fifty years ago( and we celebrate their 50th anniversary for the sacrifice they made), we must try something new, unless we want to continue bumping our heads against a stone wall.

We don't have the power to defeat them because they have too much back up, e.g., the army, navy, air force, national guard, FBI, Homeland Security, etc. At some point we will need a reconciliation or things will go from bad to worse as happened in Dallas, Texas. The nature of the panther is to strike when it is backed up against the wall or corner.

After seeing with my own eyes that there can be at least a symbiotic relationship between the people and the police, I've concluded that we need to get brothers and sisters on the police force, especially in cities where we are in the majority, and the white officers must be socialized to understand they work for the people, the people don't work for them.  The people pay their salaries but not to be brutalized and killed under the color of law. We agree with Chief Brown in Dallas who called for people to be the solution rather than the problem, to become police officers. All they need do is community consciousness, similar to the police who arrested my in Belize, Central America, when I was being deported for entering the country illegally. While I was at the police station awaiting deportation, they surrounded me and when they had me in the center of a circle, they begged me to teach them about Black Power, the real reason I was being deported. Wouldn't it be nice if the American police would ask the Black Lives Matter people to teach them about Black Power rather than try to ridicule the BLM people out of existence because just as the police ain't going nowhere, we don't think Black Lives Matter is either. Stay Woke!

Meanwhile back in Oaktown fada git down!

Activist Cat Brooks, of Oakland, is photographed near Oakland City Hall in Oakland, Calif., on Wednesday, July 1, 2015. Brooks is the founder of the Anti-Police Terror Project, co-chair of the ONYX Organizing Committee, member of Black Lives Matter Bay Area and one of the Black Friday 14. Brooks has organized several Black Lives Matter and other protests in Oakland. (Jane Tyska/Bay Area News Group) ( JANE TYSKA )

Marvin X,  poet/activist, community planner of the Black Arts Movement Business District  and Oakland Mayor Libby Schaaf who is suffering from a police prostitution scandal. She dismissed three police chiefs in nine days.  As per police/community relations, she claims the OPD has made improvements, but community activists are not satisfied with her ever since she began her tenure by meeting with the OPD rather than the community.  With the sex scandal, the OPD has obviously betrayed her faith and truth in them as protectors and servants of the community. Activists associated with the Black Lives Matter are organizing a recall. We think she might benefit with a call to Newark Mayor Ras Baraka.
--Marvin X
7/11/16

Ancestor Amiri Baraka called for the 27 city tour of the Black Arts Movement artists
to spread consciousness in the present era. In answer to ancestor AB, Marvin X is working on establishing the Black Arts Movement Business District in Oakland. Dr. Nathan Hare says, "Be careful, you're an elder then ancestor!" Marvin realizes this so he is passing the BAMBD baton to the Hip Hop generation who are the legitimate heirs of the Black Arts Movement.

 

Marvin X and Oakland City Council President Lynette McElhaney who pushed through legislation establishing the Black Arts Movement Business District in the 14th Street corridor, downtown Oakland. We thank Madam President for her effort but she was make BAMBD a priority for the mental, spiritual, cultural and economic health of Oakland.
photo Adam Turner, BAMBD

As a bold act of Kujichagulia, self-determination, what if representatives of the array of organizations and institutions in the Pan African world resolve to adopt the Red, Black and Green Flag that the Honorable Marcus Mosiah Garvey bequeathed to African people as a unifying symbol, as our Flag and proclaim August 17, Garvey’s birthday, Universal African Flag Day? 
--Ron Daniels, Institute of the Black World

The Black Arts Movement Business District calls upon the City of Oakland to display the above flag as a banner throughout the Black Arts Movement Business District immediately and without further delay, certainly, by Marcus Garvey's birthday, August 17. We further demand that the words LOVE LIFE be placed at the bottom of the banner as agreed upon by Donald Lacy, founder of the Love Live Foundation. The Oakland City Council has approved LOVE LIFE as the official motto of Oakland.


We call upon Mayor Libby Schaaf and President of the Oakland City Council, Lynette McElhaney to make this happen as a priority for the mental health of the North American African citizens of Oakland and all the citizens of Oakland. We call upon the City Council to resolve August 17 as Universal African Flag Day in Oakland. 

Black Classical music: Duke Ellington & His Orchestra - Satin Doll

Police walk off security job in protest of WNBA players support for Black Lives Matter

Minneapolis police officers walk off WNBA security detail in protest of Black Lives Matter

Maya Moore and her Minnesota Lynx teammates sported T-shirts in support of the Black Lives Matter movement on Saturday night. (David Sherman/Getty Images)

The Minneapolis Police Department’s motto is “To Protect with Courage, To Serve with Compassion.”

Except when it comes to Saturday night’s Minnesota Lynx game at the city’s Target Center, it seems.
Four Minneapolis police officers, working the game as independently contracted security personnel, walked off the job before this past weekend’s game against the Dallas Wings in response to members of the Lynx wearing T-shirts in support of the Black Lives Matter movement and calling for change in the wake of recent police shootings that left two black men dead, according to the Star Tribune.
“If we take this time to see that this is a human issue and speak out together, we can greatly decrease fear and create change,” Lynx guard, 2014 WNBA MVP and three-time league champ Maya Moore told reporters at a press conference players called prior to the game. “Tonight we will be wearing shirts to honor and mourn the losses of precious American citizens and to plea for change in all of us.”

Moore and her Lynx teammates sported black T-shirts with the words, “CHANGE STARTS WITH US … JUSTICE & ACCOUNTABILITY,” stacked on the front. On the back, the shirts featured the names Philando Castile and Alton Sterling — the two men fatally shot last week by police in Falcon Heights, Minn., and Baton Rouge, La., respectively — along with the phrase “BLACK LIVES MATTER” underneath.

Additionally, the shirts featured a Dallas Police Department emblem in honor of the five officers killed by a rogue sniper during a rally protesting the shooting deaths of Castile and Sterling. Lynx players also denounced the “senseless ambush” of the five fallen officers, according to the Star Tribune, and praised Dallas police for their efforts against the unnecessary use of deadly force in recent years.

So, it seems four Minneapolis police officers walking off a security detail for 7,613 fans in attendance at Saturday’s game was ill-advised at best and downright deplorable at worst. These officers are paid to protect and serve, albeit independently in this scenario, and one would think that should take precedence over political beliefs that clash with what was a rather reasoned take by the Lynx.
In a statement, the Lynx justifiably would not ask the officers to compromise their own beliefs, especially since they were privately contracted and the team employs other security personnel.

At the same time, the actions of the four police officers involved do not exclude them from criticism.

Making matters worse, Minneapolis Police Federation Lt. Bob Kroll, president of the city’s police union, stood firmly by the decision to leave their security post, even calling for others to do the same.
“I commend them for it,” Kroll told the Star Tribune. Adding that the four officers who walked off the job have refused to work future Lynx games and many of their colleagues have joined that lack of effort, Kroll said, “If [the players] are going to keep their stance, all officers may refuse to work there.”
In other words, the Minneapolis police union is asking WNBA players to change their stance against racial profiling if the city would like officers protecting citizens in the stands at Target Center.
This is not good. Not good at all.

According to the Star Tribune, Kroll cited “false narratives” with regard to the public’s response to police shootings of black men in recent years and warned Lynx players, “Rushing to judgment before the facts are in is unwarranted and reckless.” But shouldn’t Kroll be held to the same standard?
Let’s not forget a man was gunned down in front of his fiancée and her 4-year-old daughter by an officer at a neighboring police department, regardless of motive, and calling for change to whatever protocol ultimately left the man dead is hardly a rush to judgment, unwarranted or reckless.

Before you consider whether Castile could have also acted differently in the situation that led to his death, ask yourself if this kicker from Kroll to the Star Tribune comes from a union president who is sensitive to this issue or has no interest in opening a dialogue on black lives mattering: “They only have four officers working the event,” said Kroll, “because the Lynx have such a pathetic draw.”

There’s no doubt the Minneapolis Police Department protects with courage and serves with compassion the vast majority of the time, as most law enforcement units do in the country, but in this particular instance, it sure seems like some of them are running and hiding from the issue at hand.

Revised: Dear white people and the other white people (ignut nigguhs) : Don't ask me shit and don't tell me shit! Boycott white people!

Yes, I am boycotting white people and the other white people (ignut nigguhs) until they go into detox and long term recovery from their full blown addiction to white supremacy lunacy or mental infantile paralysis. At this time they are a danger to themselves and others, thus qualified for the mental institution.

According to ancestor Nelson Mandela, white people are the cause of global strife with their permanent wars that benefit the 1%, especially gun makers. How can America talk about violence in America when it is the number one arms supplier of the world? Ever heard of blow back? Who has the most military bases throughout the world to back up their so-called free trade capitalism, including wage slavery policies?

So Mr. and Mrs. White people and Mr. and Mrs. Other White People (ignut nigguhs), go somewhere to get you a brand new bag, go get a healing in a White Supremacy Recovery Program, then when you are clean and sober and free of any residue of white supremacy mythology (Type I and II), come talk with me, until then leave me the fuck alone with your stupid ass corny shit!
--Marvin X

Randy Weston at 90

Randy Weston at 90

Norman (Otis) Richmond aka Jalali

Randy Weston has reached the age of ninety.  Weston has been on the small planet called earth for nearly a century. He turned 90 on April 5th.

My father Norman Lee Richmond aka Bud joined the ancestors in the early 1970s. I met Weston shorty after Bud left us.  Weston has been the closest to a father to me since Bud. He has supported Diasporic Music and Saturday Morning Live on CKLN -FM 88.1 and Regent Radio.  He did fund raisers for Saturday Morning Live and Diasporic Music on CKLN-FM.

The Brooklyn, New York born Weston also has been a firm supporter of Diasporic Music on Uhuru Radio.  He offered the station copies of his classic album “Uhuru Afrika” aka Freedom Africa during several of our fund raising affairs. The pianist who calls his music “African Rhythms) not “jazz” was recorded in 1960 and was originally released on the Roulette label. Roulette Records was founded in late 1956 by Morris Levy and others. The label had known ties to New York mobsters and Levy ran the label with an iron fist.

If you have seen the 1998 film, “Why Do Fools Fall in Love” starring Halle Berry, Vivica Fox, Lela Rochon and Larenz Tate who portrayed Frankie Lymon you get an idea of what type of character Levy was. The record industry just like the United States Empire was created by gangsters.

Weston was signed by United Artists Records

Weston was signed by United Artists Records with a three year contact in 1958. He recorded a classic piece about his son “Little Niles”. Said Weston, “The reviews for that record were very favorable and I obviously wanted to record “Uhuru Afrika” for United Artists, due to the success of “Little Niles”.
The company felt he wasn’t that well-known at the time and perhaps he should do something more popular.  Said Weston, “...I thought, was that after making this more “popular” record, then I could record Uhuru.” United Artists suggested that he do a recording based on a popular100 Broadway show, which he did to no avail.

C. B. Atkins, who was Sarah Vaughan’s husband and manager at the time had links with Levy. He at one point in history was one of Muhammad Ali’s mangers.  “Atkins went to Roulette Records and talked Morris Levy into it, which was no small feat.”

Weston’s autobiography “African Rhythms” which was composed by the giant himself (he stands at 6 feet 7 inches).  It was composed by Willard Jerkins. It is a must own and read for Africa, Africans and their allies. Robin Kelley has wrote, “African Rhythms is unlike anything I’ve ever read. Randy Weston’s pianist, composer, bandleader, activist, ambassador, visionary, griot– takes the reader on a most spectacular spiritual journey from Brooklyn to Africa, around the world and back again.”

Weston traces his roots and acknowledges his ancestors                  

“He tells the story of this great music that has never been told in print tracing its African roots and branches acknowledging the ancestors who helped bring him to the music from his soul, singing praises songs for these artistic and intellectual giants whose paths he crossed, from Langston Hughes, to Melba Liston, Dizzy to Monk, Marshall Stearns to Cheikh Anta Diop.”

Meeting Fatoumata Mbengue of Senegal

Today Weston is married to Fatoumata Mbengue-Weston of Senegal. Says Weston: “In 1994 I met my African queen. I was in Paris to play a concert with the Gnawa and I was staying at a hotel near an interesting –looking African shop called Saga, which I had always meant to check out , but each time I passed by I seemed to be in a hurry or on some deadline. Even though I passed by every day, it took me a while to finally go in this shop, but somehow the Creator finally directed me there.”

Weston said he found out that Saga meant family in the Wolof language. He even went on to record an album Saga later for the France based label. The 6 foot 7 inch Weston goes on to describe Fatoumata’s shop. “She had everything you could imagine in her shop: statues, beautiful cloth, cards, jewelry, a window full of beautiful African things --- giraffes, seven-foot-tall statues … all kinds of beautiful things. She also had clothing there but nothing that would fit a big man like me. After I started going by the shop fairly frequently she arranged for her tailor to start making clothes for me because I was already wearing African clothes, but Fatou just took it to another level.”

There is an African Internationalist ending to this story. Fatoumata and Randy were married in Eqypt in a Nubian wedding. A sister from Senegal marries a brother from Brooklyn on the Nile. It would make a perfect Nollywood film.

Memorial services for Donna Jackmon, sister of Marvin X

Donna and Marvin X

Oh, Big D
I look out at the Bay waters
Amtrak to Fresno
early sat. morn
we celebrate your going home
to your Lord
from whence you came
Job said naked I came
and naked I go
Big D
we think of the good in you
and praise it
the wonderful lies you told
time after time
you so good
a nigguh would buy the Brooklyn bridge
from you
and you would sell it with that smile and grin
knowing another fool believed your lies
oh, the lies you told about me
of course I think I'm great
but you made me greater than I could imagine
never will forget when I came to Seattle
and you told your boss you couldn't come to work
you had lost contact with your brother who was in route
to Seattle in his private plane
you told your boss you lost contact with me somewhere
over Lake Tahoe
Girl, you lied so good
damn near got the whole family killed when that mafia nigguh
gave you $10,000.00 to keep for him
Big D, now who would give  you  ten thousand dollars to keep
but a damn fool you convinced with that smile, grin and funny laugh
so we'll miss your lies Big D
but we'll remember you and you know
one day I will write even more about you
the fantastic life you lived
but I know for sure
I won't be able to tell your story better than you.
Peace and Love forever
Your brother,
Marvin X
7/16/16 

Memorial Services for Donna Jackmon-Hart will be Saturday, July 16, 2PM, Cooley Funeral Home, Fresno CA. She is survived by three children: Deedra, Monte and Wendy, numerous grandchildren and great grand.

Marvin X and baby brother Tommy

Front to back: Sisters  Suzy, Debbra and Gayle

Oldest brother Ali, Debra and Judy

Black Bird Press News & Review: Race in America--the Grand Denial!

Black Bird Press News & Review: Race in America--the Grand Denial!

Wimbledon 2016: Serena Williams recites Maya Angelou poem before final

Part two: Unchained Black Hollywood/Book Panel Discussion Q&A!

Marvin X reads "Dope" by Amiri Baraka

Amiri Baraka - Dope

Amiri Baraka and Marvin X on Who Who Who Who?

 Who built this plantation house? Why would the white man build while he had free labor?

If Blacks are criminals in America, how did we get to America? Who brought us here and why?
Who was the captain on the Good Ship Jesus? Who had a miraculous conversion and wrote Amazing Grace, a song Africans should never sing? Who made us preach one sermon: Servants be obedient to your masters?
 
The white man brought us here by kidnapping us from Africa in conspiracy with ruling class Africans who benefited as much from the slave trade as the white man.
 
But who pimped us in America for four hundred years, who made us work the cotton, sugarcane and rice fields, build houses and buildings (including the White House), cook, nurse his little devil babies, who fucked our women, men and children at will on a daily basis but killed us for looking at his woman?

Who cut off our hands when we were caught reading and writing? Who assassinated us for talking about freedom, justice and equality? Who made us ignorant in public schools? Who taught us lies in school that made us believe we were lazy, docile, passive, submissive slaves who sometimes refused to work for nothing, not even a food stamp.
 

Who sold us on the auction block on New Year's Day, the most dreaded day in the life of a slave, i.e., African caught in the American slave system (Ed Howard term)? Who makes us celebrate New Year's Day in our abysmal ignorance of what that day meant to our ancestors? Who calls our celebrations and family outtings "Picknics" or Pick a Nigger and lynch him in a celebration that was often a family outing?

Who kills us daily for driving while Black, walking while Black, singing and playing music while Black? Who robs us then calls us criminals? Who aborts our babies, imprisons our men, women and children for economic crimes, mental illness and drug addiction? Who brings drugs into our communities then blames us for being drug addicts? Who kills us under the color of law but is horrified when we retaliate? Who doesn't believe what goes around comes around?
--Marvin X

SOMEBODY BLEW UP AMERICA
(All thinking people
oppose terrorism
both domestic
& international…
But one should not
be used
To cover the other)


They say its some terrorist, some
barbaric
A Rab, in
Afghanistan
It wasn't our American terrorists
It wasn't the Klan or the Skin heads
Or the them that blows up nigger
Churches, or reincarnates us on Death Row
It wasn't Trent Lott
Or David Duke or Giuliani
Or Schundler, Helms retiring

It wasn't
the gonorrhea in costume
the white sheet diseases
That have murdered black people
Terrorized reason and sanity
Most of humanity, as they pleases

They say (who say? Who do the saying
Who is them paying
Who tell the lies
Who in disguise
Who had the slaves
Who got the bux out the Bucks

Who got fat from plantations
Who genocided Indians
Tried to waste the Black nation

Who live on Wall Street
The first plantation
Who cut your nuts off
Who rape your ma
Who lynched your pa

Who got the tar, who got the feathers
Who had the match, who set the fires
Who killed and hired
Who say they God & still be the Devil

Who the biggest only
Who the most goodest
Who do Jesus resemble

Who created everything
Who the smartest
Who the greatest
Who the richest
Who say you ugly and they the goodlookingest

Who define art
Who define science

Who made the bombs
Who made the guns

Who bought the slaves, who sold them

Who called you them names
Who say Dahmer wasn't insane

Who/ Who / Who/

Who stole Puerto Rico
Who stole the Indies, the Philipines, Manhattan
Australia & The Hebrides
Who forced opium on the Chinese

Who own them buildings
Who got the money
Who think you funny
Who locked you up
Who own the papers

Who owned the slave ship
Who run the army

Who the fake president
Who the ruler
Who the banker

Who/ Who/ Who/

Who own the mine
Who twist your mind
Who got bread
Who need peace
Who you think need war

Who own the oil
Who do no toil
Who own the soil
Who is not a nigger
Who is so great ain't nobody bigger

Who own this city

Who own the air
Who own the water

Who own your crib
Who rob and steal and cheat and murder
and make lies the truth
Who call you uncouth

Who live in the biggest house
Who do the biggest crime
Who go on vacation anytime

Who killed the most niggers
Who killed the most Jews
Who killed the most Italians
Who killed the most Irish
Who killed the most Africans
Who killed the most Japanese
Who killed the most Latinos

Who/Who/Who

Who own the ocean

Who own the airplanes
Who own the malls
Who own television
Who own radio

Who own what ain't even known to be owned
Who own the owners that ain't the real owners

Who own the suburbs
Who suck the cities
Who make the laws

Who made Bush president
Who believe the confederate flag need to be flying
Who talk about democracy and be lying
WHO/ WHO/ WHOWHO/

Who the Beast in Revelations
Who 666
Who decide
Jesus get crucified

Who the Devil on the real side
Who got rich from Armenian genocide

Who the biggest terrorist
Who change the bible
Who killed the most people
Who do the most evil
Who don't worry about survival

Who have the colonies
Who stole the most land
Who rule the world
Who say they good but only do evil
Who the biggest executioner

Who/Who/Who ^^^

Who own the oil
Who want more oil
Who told you what you think that later you find out a lie
Who/ Who/ ???

Who fount Bin Laden, maybe they Satan
Who pay the CIA,
Who knew the bomb was gonna blow
Who know why the terrorists
Learned to fly in Florida, San Diego

Who know why Five Israelis was filming the explosion
And cracking they sides at the notion

Who need fossil fuel when the sun ain't goin' nowhere

Who make the credit cards
Who get the biggest tax cut
Who walked out of the Conference
Against Racism
Who killed Malcolm, Kennedy & his Brother
Who killed Dr King, Who would want such a thing?
Are they linked to the murder of Lincoln?

Who invaded Grenada
Who made money from apartheid
Who keep the Irish a colony
Who overthrow Chile and Nicaragua later

Who killed David Sibeko, Chris Hani,
the same ones who killed Biko, Cabral,
Neruda, Allende, Che Guevara, Sandino,

Who killed Kabila, the ones who wasted Lumumba, Mondlane , Betty Shabazz, Princess Margaret, Ralph Featherstone, Little Bobby

Who locked up Mandela, Dhoruba, Geronimo,
Assata, Mumia,Garvey, Dashiell Hammett, Alphaeus Hutton

Who killed Huey Newton, Fred Hampton,
MedgarEvers, Mikey Smith, Walter Rodney,
Was it the ones who tried to poison Fidel
Who tried to keep the Vietnamese Oppressed

Who put a price on Lenin's head

Who put the Jews in ovens,
and who helped them do it
Who said "America First"
and ok'd the yellow stars
WHO/WHO/ ^^

Who killed Rosa Luxembourg, Liebneckt
Who murdered the Rosenbergs
And all the good people iced,
tortured , assassinated, vanished

Who got rich from Algeria, Libya, Haiti,
Iran, Iraq, Saudi, Kuwait, Lebanon,
Syria, Egypt, Jordan, Palestine,

Who cut off peoples hands in the Congo
Who invented Aids Who put the germs
In the Indians' blankets
Who thought up "The Trail of Tears"

Who blew up the Maine
& started the Spanish American War
Who got Sharon back in Power
Who backed Batista, Hitler, Bilbo,
Chiang kai Chek who WHO W H O/

Who decided Affirmative Action had to go
Reconstruction, The New Deal, The New
Frontier, The Great Society,

Who do Tom Ass Clarence Work for
Who doo doo come out the Colon's mouth
Who know what kind of Skeeza is a Condoleeza
Who pay Connelly to be a wooden negro
Who give Genius Awards to Homo Locus
Subsidere

Who overthrew Nkrumah, Bishop,
Who poison Robeson,
who try to put DuBois in Jail
Who frame Rap Jamil al Amin, Who frame the Rosenbergs, Garvey,
The Scottsboro Boys, The Hollywood Ten


Who set the Reichstag Fire

Who knew the World Trade Center was gonna get bombed
Who told 4000 Israeli workers at the Twin Towers
To stay home that day
Why did Sharon stay away ?
/
Who,Who, Who/
explosion of Owl the newspaper say
the devil face cd be seen Who WHO Who WHO

Who make money from war
Who make dough from fear and lies
Who want the world like it is
Who want the world to be ruled by imperialism and national oppression and terror
violence, and hunger and poverty.

Who is the ruler of Hell?
Who is the most powerful


Who you know ever
Seen God?

But everybody seen
The Devil


Like an Owl exploding
In your life in your brain in your self
Like an Owl who know the devil
All night, all day if you listen, Like an Owl
Exploding in fire. We hear the questions rise
In terrible flame like the whistle of a crazy dog

Like the acid of the fire of Hell
Who and Who and WHO (+) who who ^
Whoooo and Whooooooooooooooooooooo!


AMIRI B 10/01

Video: BLACK HOLLYWOOD UNCHAINED!

Justin Desmangles, Jesse Douglas Allen Taylor, Halifu Osumare, Marvin X Jackmon, Ishmael Reed / video by Johnnie Burrell
Program: Black Hollywood Unchained
Date: July 3, 2016
Time: 1:30-3:30 PM
Location: Koret Auditorium (Lower Level of the San Francisco Public Library) 100 Larkin St.
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.

Marvin X discovered Village People Cop, Victor Willis

Village People Cop:  We Had Some Milli Vanillis in the Group!!

 

11/14/2015 BY TMZ STAFF

Victor Willis -- the cop in Village People -- is about to expose a big disco era secret, and it will forever change the way you hear "Y.M.C.A."

Willis just signed on to do an A&E/Lifetime TV movie based on his life -- and sources close to the deal tell us one of the big reveals is some Village members were lip-syncing. It's unclear exactly which of his bandmates he's calling out for faking it.

Willis was the original lead singer, but left in the early '80s on bad terms. He never performed with the group again, and even threatened to sue them for using "Y.M.C.A." in a recent TV special.
The movie, set to air sometime next year, seems timed to coincide with Victor's attempted comeback. He just released a new single and music vid.

Marvin X discovered Village People Cop, Victor Willis

In 1972, after his release from Terminal Island Federal Prison on draft related charges due to his refusal to fight in Viet Nam, Marvin X returned to San Francisco and established the Black Educational Theatre, Inc., in the Fillmore on O'farrel Street, between Fillmore and Webster. His crew of actors, musicians and dancers cleaned out an old Greek Orthodox church and transformed it into BET. His partner from Black Arts West Theatre, Ethna X. Wyatt (aka, Hurriyah Asar) who also worked with him at BET,  told him about a young man who sang daily up and down Haight Street near Scott where she lived. She urged Marvin to make contact with the young man named Victor Willis.

Marvin finally followed her advice and auditioned Victor for the lead role in the production of his myth-ritual dance drama The Resurrection of the Dead. Resurrection of the Dead was a life changing drama that included a naming rite of passage. Most of the actors kept their names for life, although Victor did not keep his name Bilal, but a now famous dancer Charlene Hunter, was renamed Jamilah and goes by that first name today. Victor as Bilal (the first muezzin or prayer caller in Islam) opened the myth-ritual dance drama with the Adhan or call to prayer, followed by such Marvin X lyrics as: Praise be the Resurrection of the Dead, Lost Queen of Egypt, Black Man Don't Wander Without Aim or Purpose and Allah Loves a Warrior.

Victor went directly from Resurrection of the Dead to roles in New York theatre and eventually lead singer and writer of the Village People. Years later he told Marvin, "It was the spiritual power in Resurrection of the Dead that gave me the energy to be successful in New York. I am forever grateful to you!"

We are so happy to hear Victor is making a come back! It will be The Resurrection of the Dead!
--Marvin X

Marvin X

photo Spencer Wilkerson

Neely Fuller, Jr.: If you don't understand white supremacy...everything else will only confuse you

 

Black people, we are the most unscientific people on the planet. Yet, we harbor some of the most outlandish, untested, heavily opinionated pseudo-intellectual jargon riddled and irrelevant information on the face of the planet earth.

The scientific method has four steps:

1. Observation and description of a phenomenon or group of phenomena.

2. Formulation of an hypothesis to explain the phenomena. In physics, the hypothesis often takes the form of a causal mechanism or a mathematical relation.

3. Use of the hypothesis to predict the existence of other phenomena, or to predict quantitatively the results of new observations.

4. Performance of experimental tests of the predictions by several independent experimenters and properly performed experiments.

Can we PLEASE step away from all this mind-numbing nonsense and FINALLY get SERIOUS about ending our condition?

RBG| WHITE SUPREMACY 2 -In A Crazy House Called America- Marvin X

Marvin X At the Black Caucus of California Community Colleges

Marvin X at the San Francisco's Juneteeth 2016 in Fillmore

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

Encyclopedia of Aging | 2002 | Wells, David G.

COPYRIGHT 2002 The Gale Group Inc.

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 storage—or 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): 331–356.
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 1–88.
Davis, H. P., and Squire, L. R. "Protein Synthesis and Memory: A Review." Psychology Bulletin 96 (1984): 518–559.
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): 4363–4367.
Foster, T. C. "Involvement of Hippocampal Synaptic Plasticity in Age-Related Memory Decline." Brain Research Review 30 (1999): 236–249.
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): 870–873.
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): 2262–2267.
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): 24–30.
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): 1147–1157.

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Neural plasticity: consequences of stress and actions of antidepressant treatment

Ronald S. Duman, PhD^*

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This article has been cited by other articles in PMC.

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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.

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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.

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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 hippocampus^15,16 (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.

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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.

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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.

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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-HT_1A 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-HT_1A 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-HT_1A 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.

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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).

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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.

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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.

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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-HT_1A) 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

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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.

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Selected abbrewiations and acronyms

BDNF	brain-derived neurotrophic factor
cAMP	cyclic adenosine monophosphate
CaRE	cAMP response element
CREB	cAMP response element binding protein
FGF-2	fibroblast growth factor-2
5-HT	5 -hydroxy tryptamine (serotonin)
LTP	long-term potentiation
NMDA	N-methyl-D-aspartate
PDE4	phosphodiesterase type IV
PKA	protein kinase
SSRI	selective serotonin reuptake inhibitor

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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.

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