Deaths from Marijuana v. 17 FDA-Approved Drugs (Jan. 1, 1997 to June 30, 2005

Deaths from Marijuana v. 17 FDA-Approved Drugs

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Fashion show to increase awareness and support of bipolar disorder research

Fashion show to increase awareness and support of bipolar disorder research

The May 21^st event benefits the Prechter Research Fund at the University of Michigan Depression Center

 

Melvin McInnis & Wally Prechter

Meet the expert:  Melvin McInnis, M.D., Thomas B. and Nancy Upjohn Woodworth Professor of Bipolar Disorder and Depression in the Department of Psychiatry Learn more:  U-M Depression Center bipolar information  Prechter Bipolar Research Fund Download images

ANN ARBOR, Mich. - Can’t buy a new yacht? No biggie. You can still get the fabulous lounge clothes.

 

Italian designer Gimmo Etro’s exotic print dresses and other fashions will be available for viewing at a runway show at Saks Fifth Avenue at Somerset Collection in Troy.

 

The runway show hopes to shine a spotlight on bipolar disorder, one of the most prevalent and least talked about mood disorders in the United States. It will also benefit the Heinz C. Prechter Bipolar Research Fund at the University of Michigan Depression Center. 

 

The show, which opens at 6:30 p.m. May 21, will include a reception and brief remarks about breakthrough bipolar disorder research conducted at the University of Michigan Depression Center. Funds raised in conjunction with this event will help advance critically needed research already underway at the Center.

 

“Research being conducted by the Prechter Bipolar Research team is helping us better understand bipolar disorder, find more effective treatments, and get us closer to a cure,” says Melvin McInnis, M.D., Thomas B. and Nancy Upjohn Woodworth Professor of Bipolar Disorder and Depression in the Department of Psychiatry. 

 

Research features a genetic repository where DNA samples from individuals with bipolar disorder and those unaffected by the disease are collected and studied. The DNA will be evaluated to find clues to early diagnosis and a “roadmap” to understanding causes and identify treatments, McInnis explains.

 

Saks Fifth Avenue will provide a glitzy evening of fashion and high style for guests. Their generous sponsorship, along with the iconic fashions provided by ETRO, has created the opportunity to raise awareness about bipolar disorder as well as funding for research.

 

"I would like to express my gratitude to Saks Fifth Avenue for supporting the work of the Heinz C. Prechter Bipolar Research Fund by hosting a Fashion Show,” says Waltraud “Wally” Prechter, founder of the Heinz C. Prechter Bipolar Research Fund. “The proceeds will benefit the Gene Repository, a one-of-a-kind project in our nation. I am delighted and hopeful that by combining fashions and fundraising, we will be able to accelerate research and understand this insidious illness."

 

Mrs. Prechter has worked tirelessly to promote the bipolar disorder cause since the death of her husband Heinz C. Prechter in 2001. Mr. Prechter was a successful and celebrated automotive executive and philanthropist who fell victim to suicide after suffering from bipolar disorder for most of his adult life.

 

Tickets for the event are $150 and sponsorships in the amounts of $1,000, $5,000 and $10,000 are also available. To learn more about the fashion show, please contact the Prechter Bipolar Research Fund at (734) 675-2200. For more general information about the Fund, please visitwww.prechterfund.org.

 

Facts about the Prechter Genetic Repository and the Heinz B. Prechter Bipolar Research Fund at the University of MichiganDepressionCenter:

• The fund has supported research at U-M, Stanford University and Cornell University.
• The repository has expanded with the addition of genetic samples and data from 1,500 patients collected by Johns Hopkins University researchers who will now work with the other Prechter-funded researchers.
• Many more DNA samples are needed, both from people who have bipolar disorder and from people without the disorder, no matter whether they have loved ones with bipolar.
• Giving a DNA sample involves allowing the research team to take a small sample of blood. Volunteers are interviewed at the start of the study, and annually after that, about their health, mental well-being and other issues.
• Those interested in finding out more about the project can call toll-free 1-877-UM-GENES or  (1-877-864-3637), or e-mail bpresearch@umich.edu.

Facts about bipolar disorder:

• Bipolar disorder was once called manic depression, but the term “bipolar disorder” is more commonly used today.
• The main characteristic of bipolar disorder is major mood swings, which can occur off and on throughout life. These can alternate between manic “up” or “high” periods, and depressed “down” or “low” periods.
• More than 5.7 million Americans, or 2.6 percent of the population, are estimated to have some form of bipolar disorder.
•  Bipolar disorder runs in families, and children whose parents have it are at an increased risk of developing it themselves.
•  Suicide or suicide attempts are an unfortunate but common occurrence among people with bipolar disorder.

Find more information about bipolar disorder:

• U-M Depression Center bipolar information: www.med.umich.edu/depression/bipolar.ht
• Prechter Fund and Prechter Genetic Repository at the U-M Depression Center: www.prechterfund.org
• National Institute of Mental Health Bipolar information: www.nimh.nih.gov/publicat/bipolar.cfm
• Depression & Bipolar Support Alliance: http://www.dbsalliance.org/site/PageServer?pagename=about_bipolar_overview

The University of Michigan Depression Center is the nation’s first comprehensive center dedicated to patient care, research, education and public policy in depression and bipolar disorder. Established in 2001, its mission is fivefold: to detect depression and bipolar disorders early, treat them earlier and more effectively, prevent recurrences and progression, counteract stigma, and improve public policy. More than 200 faculty, staff and students from across the University are members of the center. For more information about the University of Michigan Depression Center, please visit our web site atwww.depressioncenter.org or contact us at 800-475-UMICH.

Genetic Breakthrough for Bipolar Disorder

In what amounts to a scientific breakthrough a combined team of scientists from Britain and the United States have located two genes linked to bipolar disorder. Professor Nick Craddock, of Cardiff University's school of medicine, who lead the research says, "the findings will help people to avoid saying bipolar is just the way some people are, or that they should be able to control it . . . it puts it on a parallel with other diseases, such as heart disease and diabetes."

 

In one of the largest research projects of its kind, genes from more than 10,000 people, including 4,300 with bipolar disorder were examined, constituting a review of around 1.8 million genetic variations. The research team then identified that people with bipolar disorder were significantly more likely to have variants of the ANK3 and CACNA1C genes. These genes help to make proteins that control the flow of calcium and sodium ions that move in and out of nerve cells.

 

The ANK3 gene has a role in controlling the activity of cells whereas the CACNA1C gene is responsible for channels that control calcium flow from the brain. Normal brain function relies on a delicate balance of sodium and calcium. "The brain operates according to how quickly calcium and sodium are going in and out of cells and how much of it goes in and out," Craddock said.

 

The study, reported in the journal of Nature Genetics, is not expected to be helpful in determining risk for the disorder. Many people have the genes but do not have bipolar disorder. What the findings do achieve is they put to rest the notion that bipolar is purely psychological in nature. The fact that the disorder can now be identified as physiological will also help to provide a focus for future research and give direction to new treatments. Although lithium is known to help, it only achieves benefits for two-thirds of people and can cause weight gain and shakiness.

 

In an upbeat assessment of work to date and speaking to journalist Madeline Brindley of the Western Mail, Professor Craddock stated:

 

"When the research team can identify bipolar as an illness, like any other caused by a genetic predisposition, the stigma and discrimination faced by people with bipolar may finally be able to become a thing consigned to the history books."

Emerging Clinical Applications for Cannabis & Cannabinoids

Emerging Clinical Applications For Cannabis & Cannabinoids
A Review of the Recent Scientific Literature, 2000 — 2009

Despite the ongoing political debate regarding the legality of medicinal marijuana, clinical investigations of the therapeutic use of cannabinoids are now more prevalent than at any time in history. A search of the National Library of Medicine's PubMed website quantifies this fact. A keyword search using the terms "cannabis, 1996" (the year California voters became the first of 13 states to allow for the drug’s medical use under state law) reveals just 258 scientific journal articles published on the subject during that year. Perform this same search for the year 2008, and one will find over 2,100 published scientific studies.

While much of the renewed interest in cannabinoid therapeutics is a result of the discovery of the endocannabinoid regulatory system, some of this increased attention is also due to the growing body of testimonials from medicinal cannabis patients and their physicians. Nevertheless, despite this influx of anecdotal reports, much of the modern investigation of medicinal cannabis remains limited to preclinical (animal) studies of individual cannabinoids (e.g. THC or cannabidiol) and/or synthetic cannabinoid agonists (e.g., dronabinol or WIN 55,212-2) rather than clinical trial investigations involving whole plant material. Predictably, because of the US government's strong public policy stance against any use of cannabis, the bulk of this modern cannabinoid research is taking place outside the United States.

As clinical research into the therapeutic value of cannabinoids has proliferated – there are now more than 17,000 published papers in the scientific literature analyzing marijuana and its constituents — so too has investigators' understanding of cannabis' remarkable capability to combat disease. Whereas researchers in the 1970s, 80s, and 90s primarily assessed cannabis' ability to temporarily alleviate various disease symptoms — such as the nausea associated with cancer chemotherapy — scientists today are exploring the potential role of cannabinoids to modify disease.

Of particular interest, scientists are investigating cannabinoids' capacity to moderate autoimmune disorders such as multiple sclerosis, rheumatoid arthritis, and inflammatory bowel disease, as well as their role in the treatment of neurological disorders such as Alzheimer's disease and amyotrophic lateral sclerosis (a.k.a. Lou Gehrig's disease.)

Investigators are also studying the anti-cancer activities of cannabis, as a growing body of preclinical and clinical data concludes that cannabinoids can reduce the spread of specific cancer cells via apoptosis (programmed cell death) and by the inhibition of angiogenesis (the formation of new blood vessels). Arguably, these latter trends represent far broader and more significant applications for cannabinoid therapeutics than researchers could have imagined some thirty or even twenty years ago.

THE SAFETY PROFILE OF MEDICAL CANNABIS

Cannabinoids have a remarkable safety record, particularly when compared to other therapeutically active substances.  Most significantly, the consumption of marijuana – regardless of quantity or potency -- cannot induce a fatal overdose. According to a 1995 review prepared for the World Health Organization, “There are no recorded cases of overdose fatalities attributed to cannabis, and the estimated lethal dose for humans extrapolated from animal studies is so high that it cannot be achieved by … users.”

In 2008, investigators at McGill University Health Centre and McGill University in Montreal and the University of British Columbia in Vancouver reviewed 23 clinical investigations of medicinal cannabinoid drugs (typically oral THC or liquid cannabis extracts) and eight observational studies conducted between 1966 and 2007.  Investigators "did not find a higher incidence rate of serious adverse events associated with medical cannabinoid use" compared to non-using controls over these three decades.

That said, cannabis should not necessarily be viewed as a ‘harmless’ substance.  Its active constituents may produce a variety of physiological and euphoric effects. As a result, there may be some populations that are susceptible to increased risks from the use of cannabis, such as adolescents, pregnant or nursing mothers, and patients who have a family history of mental illness. Patients with Hepatitis C, decreased lung function (such as chronic obstructive pulmonary disease), or who have a history of heart disease or stroke may also be at a greater risk of experiencing adverse side effects from marijuana. As with any medication, patients should consult thoroughly with their physician before deciding whether the medicinal use of cannabis is safe and appropriate.

HOW TO USE THIS REPORT

As states continue to approve legislation enabling the physician-supervised use of medicinal marijuana, more patients with varying disease types are exploring the use of therapeutic cannabis. Many of these patients and their physicians are now discussing this issue for the first time, and are seeking guidance on whether the therapeutic use of cannabis may or may not be advisable. This report seeks to provide this guidance by summarizing the most recently published scientific research (2000-2009) on the therapeutic use of cannabis and cannabinoids for 19 clinical indications:

* Alzheimer's disease
* Amyotrophic lateral sclerosis
* Chronic Pain 
* Diabetes mellitus
* Dystonia 
* Fibromyalgia 
* Gastrointestinal disorders
* Gliomas 
* Hepatitis C 
* Human Immunodeficiency Virus 
* Hypertension 
* Incontinence 
* Methicillin-resistant Staphyloccus aureus (MRSA)
* Multiple sclerosis
* Osteoporosis 
* Pruritus 
* Rheumatoid arthritis
* Sleep apnea 
* Tourette's syndrome

In some of these cases, modern science is now affirming longtime anecdotal reports of medicinal cannabis users (e.g., the use of cannabis to alleviate GI disorders). In other cases, this research is highlighting entirely new potential clinical utilities for cannabinoids (e.g., the use of cannabinoids to modify the progression of diabetes.)

The conditions profiled in this report were chosen because patients frequently inquire about the therapeutic use of cannabis to treat these disorders. In addition, many of the indications included in this report may be moderated by cannabis therapy. In several cases, preclinical data and clinical indicates that cannabinoids may halt the progression of these diseases in a more efficacious manner than available pharmaceuticals. In virtually all cases, this report is the most thorough and comprehensive review of the recent scientific literature regarding the therapeutic use of cannabis and cannabinoids.

For patients and their physicians, let this report serve as a primer for those who are considering using or recommending medicinal cannabis. For others, let this report serve as an introduction to the broad range of emerging clinical applications for cannabis and its various compounds.

Paul Armentano
Deputy Director 
NORML | NORML Foundation
Washington, DC
January 15, 2009

* The author would like to acknowledge Drs. Dale Gieringer, Gregory Carter, Steven Karch, and Mitch Earleywine, as well as Bernard Ellis, MPH, NORML interns John Lucy, Christopher Rasmussen, and Rita Bowles, for providing research assistance for this report. The NORML Foundation would also like to acknowledge Dale Gieringer, Paul Kuhn, and Richard Wolfe for their financial contributions toward the publication of this report.

** Important and timely publications such as this are only made possible when concerned citizens become involved with NORML. For more information on joining NORML or making a donation, please visit: http://www.norml.org/join. Tax-deductible donations in support of NORML's public education campaigns should be made payable to the NORML Foundation.

Endocannabinoid System Regulates Emotional Homeostasis, Study Says

Endocannabinoid System Regulates Emotional Homeostasis, Study Says
Category: News and Politics

Madrid, Spain: Naturally occurring chemicals in the human body that mimic the effects of plant cannabinoids moderate human emotions and control anxiety, according to findings published in the Spanish scientific journal Revista de Neurologica.

Investigators at Complutense University in Madrid report that manipulating of the endocannabinoid system may one day be a course of treatment in the management of certain emotional disorders.

"[P]resent data reinforce the involvement of the endocannabinoid system in the control of emotional homeostasis and further suggest the pharmacological manipulation of the endocannabinoid system [is] a potential therapeutic tool in the management of anxiety-related disorders," authors concluded.

Previous research on the endocannabinoid system indicates that endogenous cannabionoids moderate numerous biological functions, including appetite, blood pressure, reproduction, motor coordination, and bone mass.

For more information, please contact Paul Armentano, NORML Deputy Director, at: paul@norml.org. Full text of the study, "Functional role of the endocannabinoid system in emotional homeostasis," appears in the January issue of Revista de Neurologica.

CANNABIS AND THE BRAIN

CANNABIS AND THE BRAIN: Iversen, L, Brain. 2003; 126: pp. 1252-1270. A large literature exists on the effects of cannabis,this review focuses mainly on the more recent literature in this field.

In 1990 Israeli scientists discovered 'receptors' in the human brain which are uniquely suited for cannabis. In 1992 a special protein binder was identified.

Cannabis acts on specific cannabinoid receptors in the brain. Such receptors have been found in humans, in rats, chickens, turtles, trout and possibly even in fruit flies.

This distribution may suggest that the gene responsible must have been present early in evolution, and its conservation implies that the receptor serves an important biological function.

Since THC is not a naturally occurring substance within the brain, the existence of a cannabinoid receptor implied the existence of a naturally occurring or 'endogenous' cannabinoid-like substance. A brain molecule which binds to the receptor was identified (by Devan in 1992). The molecule is called arachidnylethanolamide and is fat soluble like THC. It has been called anandamide from the Sanskrit word meaning bliss' This substance has no effect on cells which do not have the receptor. The biological role of the anandamide molecules remain unknown. (Above extracted from Australian Government Report)

The action of cannabis in the brain is completely different to the actions of hard drugs. The latter effect levels of a chemical called dopamine which occurs naturally in the brain. This is the chemical which enables us to feel pleasure. Heroin and cocaine and derivatives repress the production of dopamine. The pleasure or high of the drug is caused by artificially boosting the pleasure centres. When the drug wears off the natural dopamine production is lowered and the user wants more drug. This is particularly true of cocaine where the high is short lived. A snort of cocaine usually makes one want another line soon. Long term use of hard drugs has a more disastrous effect and abstinence produces withdrawal symptoms, the user often unable to feel any pleasure at all.

Many people who use cannabis think they simply do so for the buzz. In fact cannabis is not only a medicine which makes people well, it is also a preventative medicine. Some people seem miserable or even angry when their supply of cannabis runs out; this is because that is how they used to be before taking cannabis.

A very few people have allergic reactions to cannabis. Some of these are to grass and not to hash. Even fewer people have negative metal effects - sometimes wrongly called 'cannabis psychosis'. These reports are complicated because the person has sometimes consumed other substances such as cocaine or LSD at the same time as cannabis or in the past and have not reported it to their doctor, so cannabis gets the blame. Other complications are the impurities in the cannabis and a possibly unbalanced mind to start with.

THE RECEPTOR

TAMPA, Fla., June 9 /PRNewswire/ --
In Dr. Thomas Klein's crowded laboratory office, beneath the shelves of scientific journals hangs a preserved puffer fish with an imitation joint dangling from its mouth.

Even the ancient blowfish has been found to harbor chemical receptors that react to delta-9 tetrahydrocannabinol, or THC, the compound in marijuana that produces a high said Dr. Klein, professor of medical microbiology and immunology at the University of South Florida.

"It's fascinating," he said. "Why would both humans and this fish evolve with the genes for a receptor that would only be activated if you smoked marijuana? Conservation through evolution suggests that the gene is important.

"We now know there's a substance circulating in the body called anandamide that binds to cannabinoid receptors. So there's definitely a physiological role for endogenous cannabinoid receptors, possibly in behavior modification or defining moods as well as regulating immunity and other functions."

Dr. Klein is a pioneer in the new field of psychoneuroimmununology. He studies physical links between drugs of abuse and the brain, emotions and immunity.

Supported by a $674,000 National Institutes of Health grant, he heads one of few scientific groups in the world investigating the function of cannabinoid (marijuana) receptors in the immune system. Cannabinoid receptors have also been found in the brain, the gut and the reproductive system.

Cells imbedded with these receptors are inhibited from functioning when exposed to the THC molecule.

Pot's influence on the immune system continues to be hotly debated within the medical community. Animal and human studies have demonstrated that virtually every immune function, from antibody production to the destruction of invading microorganisms, is suppressed by relatively high concentrations of marijuana. In those whose immune responses are already poor, marijuana may aggravate deteriorating health.

"It's believed to be a rather benign drug, effective in reducing pain and nausea," Dr. Klein said, "but scientific evidence is accumulating, through the study of the cannabinoid receptor system, that THC might affect almost every cell in the body.

"People need to know that if they smoke marijuana, they are not just altering their moods. They're altering their immune systems."

Scientists may know more about marijuana's hazards or benefits to health once they understand how the cannabinoid system fits into the body's complex network of immune regulation.

Dr. Klein suspects the natural purpose of cannabinoid receptors may be to control more powerful immune systems serving as the body's first line of defense against infection or tumors.

"The horse gets the buggy started, but the cannabinoid system is like the driver with the whip who keeps things going," he said.

A BRAIN SHIELD FROM--WELL, MARIJUANA

From : Business Week, November 4, 1996, Pg. 199

The first drug to curtail the spread of brain damage resulting from strokes and head or spinal cord injuries has entered clinical tests at six hospitals in Israel. Its key ingredient is dexanabinol, a synthetic molecule based on the active agent in marijuana. Dexanabinol was discovered six years ago by Raphael Mechoullam, a researcher at Hebrew University in Jerusalem, and developed by the Rehovot (Israel) research arm of Pharmos Corp. in Alachua, Fla.

Dexanabinol has two novel properties: It can cross the so-called blood-brain barrier that prevents foreign molecules from entering the brain. And once in, the drug appears to halt the brain-cell deterioration that follows a blow to the head or a stroke. In four years of animal testing, the drug produced "outstanding" results, says Michael Schickler, vice-president of Pharmos' Israel operations. Pharmos expects clinical tests to be completed by the end of 1997. If it works, dexanabinol could hit the market by 2000.

CANNABIS AND I.Q.

The Coptic Study of 1981 stated: 
...I.Q.'s of Zion Coptics increased after they began to use ganga

Messengers of the Brain

by Marcia Purse

You're taking Prozac, and you've heard it described as an SSRI. Maybe you know that SSRI stands for selective serotonin reuptake inhibitor. But that's quite a mouthful -- what does it mean?

In other pages on this site, we look at medications that are commonly prescribed for mood disorders, such as manic depression. Included in these reviews is a brief description of how each functions -- or is thought to function, since many are still being studied.

In order to make sense of any of this, it is necessary to understand something about how impulses are transferred from one nerve to the next, since medications such as mood stabilizers, antidepressants and antipsychotics all affect this process to bring about changes. In this article, I will give a brief, simplified description of how the brain's message carriers (neurotransmitters) operate, and then try to clarify the process by telling the illustrated story, "GABAs in the 'Hood." *

Neurotransmitters

There are several of these, but the ones that are most related to mood disorders are:

• The monoamines - serotonin, norepinephrine and dopamine
• GABA (gamma amino butyric acid)
• Glutamate

Others that come into play, with some side effects, are acetylcholine, which transmits orders to the muscles, and histamine, which has a lot to do with allergies, appetite regulation, weight gain (for those on certain medications), and sleep quality.

When a message comes in at one end of a nerve cell, an electrical impulse travels down the "tail" of the cell, called the axon, and causes the release of the appropriate neurotransmitter. Molecules of the neurotransmitter are sent into the tiny space between nerve cells, called the synaptic cleft. There, one or more of the following can occur for each molecule:

1. It may bind (attach) to the receptors in the adjacent nerve cell, send the message on, leave the receptor, then repeat this process or go on to one of the other steps.
2. It may hang around in the synapse until a receptor becomes available, bind to it, release, and continue with steps 1 to 3 until its activity is ended by steps 4, 5 or 6.
3. It may bind to the first cell's autoreceptors, which tell that cell not to release any more of the neurotransmitter molecules, then leave the autoreceptor and continue trying to bind again somewhere until its activity is ended by step 4, 5 or 6.
4. It may be rendered inactive by an enzyme.
5. It may be reabsorbed by the first cell in the "reuptake" process, and recycled for later use or deactivated.
6. It may diffuse out of the synapse and be deactivated elsewhere.

Now, so many things can go wrong with this process that it's not surprising mood disorders are fairly common. For example:

• The nerve cells (neurons) might not be manufacturing enough of a neurotransmitter.
• Too many molecules of the neurotransmitter may be dissolved or deactivated by enzymes.
• Too much of a neurotransmitter may be released.
• The molecules may be reabsorbed too quickly by the reuptake transporters.
• The autoreceptors may be activated too soon, shutting down the release of neurotransmitter molecules prematurely.

Or there could be some other circumstance involving electrically charged particles of potassium, sodium, chloride or calcium. It's enough to make your head hurt, isn't it?

Here, let's look at it another way.

Communication at Brain Complex, or "GABAs in the 'Hood"

To start with, look at Figure 1, which is a very simplified drawing of a synapse.

Figure 1


Figure 2
For our story, let's change the components shown above into something more familiar -- parts of a neighborhood. The two neurons are Building A and Building B of Brain Complex. They are separated by a narrow street (the synaptic cleft). The GABA terminal button is now a motor pool. Each vesicle containing neurotransmitter molecules becomes a minibus filled with GABA Team messengers. The receptors and autoreceptor become phone booths. The reuptake transporter, where neurotransmitters are sucked back in to be recycled, changes to an inviting coffee shop. And the enzymes are assassins on motorcycles. (No offense meant to motorcycle lovers!)

So over in Building A, the driver of each minivan gets a call from the front office (that's the neuron's cell body, not shown) on his cell phone: "Send this Message over to Building B!" And right away things start to happen.

Figure 3

Immediately the drivers take their vehicles (that is, vesicles) to the garage exit and release the GABA Team messengers (neurotransmitters) into the street (synaptic cleft) between Building A (the sending neuron) and Building B (the receiving neuron). Like sprinters, the GABAs take off quickly, each looking for a phone booth that matches his or her uniform (they could not get into any other color booth). Gertrude, Gerald and Gloria get there first. Quickly each slips into a booth (Figure 4) and makes a call into the office (cell body) of Building B, relaying the Message. Then each backs out and looks for another booth. All the GABA messengers are elbowing each other out of the way (and dodging motorcycles) to get into the available booths and make the same call if they get in.

Figure 4
But there are some traps and hazards for the GABA team. George GABA never makes it to Building B at all -- he has been knocked unconscious by a motorcycle-riding assassin (enzyme). His color change denotes that he has forgotten the message now -- in essence, he has been "deactivated."

Meanwhile, Glenn GABA has gone to the phone booth attached to Building A. "There's too many of us out here," he tells the front office. "Don't send any more." Then he, too, goes back out into the street. When the front office gets enough similar calls, the minivan drivers will be told to return to the motor pool and not send any more messengers out.

And then there is that seductive coffee shop (reuptake transporter) on the other corner of Building A. If a messenger gets close enough to smell the heavenly aroma of fresh coffee and doughnuts, he or she will surely be sucked in, and once inside, will be refreshed and then return to the motor pool to await the next assignment. Eventually all the surviving GABAs will return home via the coffee shop.

The whole event has taken no more than a millisecond.

---

Now as you have probably realized, it isn't really this simple. But this illustration will give you a basic idea of how neurotransmitters operate and why it is so important that they operate correctly. It's crucial that neither too many nor too few of them are released into the cleft, the autoreceptors and enzymes are working properly, and that a myriad of other factors fall into place to contribute to a healthy process. When they don't, you can get illnesses like Parkinson's, which is caused by a dopamine deficiency; or you may have tetanus, which prevents the release of GABA and can be fatal if breathing muscle control is lost. Or you might have schizophrenia, which is thought to be caused by an imbalance of dopamine, or epilepsy, apparently caused in part by an overabundance of GABA.

My goal with "GABAs in the 'Hood" has been to provide an easy-to-understand description of basic neurotransmitter functions. Remember the team messengers and their adventures in the 'hood as you read other articles!


_{Thanks to Richard Schuergar, Former About Guide to Neuroscience, for his contributions to this article.}