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A Beginner's Guide to Psychopharmacology

Posted by DSCH on September 25, 2003, at 15:31:58

In reply to Does this site exist?, posted by Wildflower on September 25, 2003, at 11:28:13

DISCLAIMER

I have a master's degree in an applied science discipline that is NOT pharmacology. Please, for your own well being do not do anything on your own iniative based upon what I have written here without consulting your psychiatrist first. Also, be aware that psychiatrists can become wary if you bring up drugs by name, self-diagnose yourself, and/or mention psychopharmacological particulars. They may interperet these as warning signs of "drug-seeking behavior" and it can set you back in your treatment and working relationship. Remember, that is what THEIR job is supposed to be! What is written here is also not guaranteed to be completely correct. Psychopharmacology is an evolving field as is the neuroscience of psychiatric disorders and their treatment. I am also a falable human being just like everybody else. In the interests of brevity and simplicity I am not going to go into the fullest detail that I can. Alright, with that out of the way...

NEUROTRANSMITTERS

A neurotransmitter is a molecule that is stored within vessicles (storage vessels) inside nerve cells (neurons) that gets released and travels across the gaps that separate them (the synaptic gaps). After crossing the synaptic gap, they temporarily bind into and stimulate sites called receptors. In this fashion a message gets transfered from one neuron (the releasing one) to the other (the one with the stimulated receptor).

There are several major neurotransmitter types within the brain and central nervous system (CNS) that are of particular interest. There are many more than I will list here, but these are the ones most psychoactive medications are targeted at:

A) Serotonin (5HT)
B) Norepinepherine (NE), aka Noradrenaline
C) Dopamine (DA)
D) Gamma-aminobutyric acid (GABA)

A chart describing what these are currently understood to affect by their relative deficiency or overabundance within the synaptic gaps can be found here (courtesy of Blake Graham)...

http://www.nutritional-healing.com.au/neurotransmitters.htm

OK, say we want to target one or more of these neurotransmitters and either give their associated messages either a boost or a reduction in signal. The ways you can do this are: (1) release stimulation, (2) inhibiting reuptake, (3) receptor agonizing, (4) receptor antagonizing, and (5) oxidation inhibition.

(1) RELEASE STIMULATION

A drug can be introduced that stimulates neurons to release more neurotransmitters of a given type from their vessicles each time a message needs to be conveyed. The greater number of molecules released leads to more stimulated receptors and hence a boosted signal. Note that if the vessicles are unable to keep up with the increased demand, this tactic isn't going to accomplish much, so your results from this sort of drug are limited by your processing of amino acids to synthesize the neurotransmitters in the first place.

Psychostimulants such as the amphetamines (Adderal, Dexedrine, Desoxyn, etc), methylphenidate (Ritalin), and pemoline (Cylert) stimulate the release of dopamine, norepinepherine, or both. This is not all they can do however.

(2) INHIBITING REUPTAKE

Some of the molecules released from the vessicles to relay a message are sucked back in before they can cross the synaptic gap. This is called 'reuptake'. A reuptake inhibitor is supposed to reduce the chances of this ocurring, thus causing an increase in available neurotranmitters in the gap and a boost in signal.

Tricyclics are a structurally similar group of drugs that can inhibit reuptake of both serotonin and norepinpherine in varying degrees (in addition to antagonizing receptors as which is discussed in (4) below). Selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine (Prozac) are very aptly named. Atomoxetine (Strattera) is an example of a selective norephinepherine reuptake inhibitor. Venlafaxine (Effexor) inhibits uptake of first serotonin; then both serotonin and norepinepherine; then serotonin, norepinepherine and dopamine as its dosage is increased.

(3) RECEPTOR AGONIZING

A drug can introduced that will temporary bind into given types of receptor(s) and stimulate it/them, thus acting as a stand-in for the associated neutrotransmitter molecule and increase signal.

BZD agonists, "benzos", agonize GABA receptors.

(4) RECEPTOR ANTAGONIZING

A drug can introduced that will temporarily bind into given types of receptor(s), but NOT stimulate it/them and also shield the receptor(s) from being stimulated by the upstream neuron's own neurotransmitters while it is bound in. You can decrease a signal in this fashion.

Many antipsychotics are dopamine receptor anatagonists. Many of the side effects of the tricyclics are due to their antagonism of a wide range of receptors.

(5) OXIDATION INHIBITION

Enzymes are present in the brain that breakdown (oxidize) free floating neurotransmitters so that they do not build up within the synaptic gaps too much. It would appear that for some people this process is too active.

Monoamine oxidase-A (MAO-A) and monamine oxidase-B (MAO-B) are responsible for scavaging serotonin, norepinepherine, and dopamine in addition to other duties within the body. Irreversible inhibition of both MAO-A and MAO-B is what the MAOIs such as Nardil and Parnate do. Reversible inhibition of just MAO-A is called RIMA and commerically only moclobemide (Manerix) and toloxatone (Humoryl) do this (though selegiline below ~10-15 mg/day has been claimed to do this as well). The potentially fatal "Cheese Crisis" effect and dangerous drug interactions are a downside to the MAOIs that are dodged by RIMAs, but RIMAs themselves appear to have not met with much acceptance outside Europe.

BRAIN REREGULATION IN RESPONSE TO MEDICATION

The density of receptors has been seen to change over a period of weeks in response to the reuptake inhibiting medications which correlates with their often delayed-action efficacy, so simply raising or lowering of the number of neurotransmitter molecules available in the synaptic gaps would appear not to be the full story behind why they work. However, other classes can "kick in" immediately. Then there are side effects, "poop out", and paradoxical reactions. And that this point I will bow out as I don't understand these enough to write much more than that and this is getting long enough as it is. I will add that each individual, by having their own DNA sequence coding for a unique structural and metabolic system, as well as having a unique life history that has affected that structure and metabolism, has the potential for unique responses to psychoactive medication.

MORE INFO

A very useful chart that has trade names and active mechanisms listed for very many psychoactive medications has been maintained by SLS...

http://sl.schofield3.home.att.net/medicine/psychiatric_drugs_chart.html

Once you find a specific medication you are interested in, Google it and prepare for information overload! Don't believe everything you read, however, and your mileage may vary (YMMV). Good luck.


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poster:DSCH thread:263190
URL: http://www.dr-bob.org/babble/20030923/msgs/263264.html