![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 19 of 19. This is the beginning of the thread.
Posted by Wildflower on September 25, 2003, at 11:28:13
I'm still pretty new to this board and I'm honestly frustrated that I can't understand some of the medical posts.
Is there a website that I can refer to that would explain the difference between MAOIs, SSRIs, mood stabilizers and anxiety meds and also provide me with prescription names? I'm going back to my pdoc in a few weeks and I want to be armed with knowledge regarding possible treatment options for my depression and SAD.
Thank you soooo much!
Posted by wsj on September 25, 2003, at 12:23:54
In reply to Does this site exist?, posted by Wildflower on September 25, 2003, at 11:28:13
intellihealth
webmd
pdror just do a google search on maoi or ssri
Posted by Michelle0202 on September 25, 2003, at 13:08:44
In reply to Does this site exist?, posted by Wildflower on September 25, 2003, at 11:28:13
> I'm still pretty new to this board and I'm honestly frustrated that I can't understand some of the medical posts.
>
> Is there a website that I can refer to that would explain the difference between MAOIs, SSRIs, mood stabilizers and anxiety meds and also provide me with prescription names? I'm going back to my pdoc in a few weeks and I want to be armed with knowledge regarding possible treatment options for my depression and SAD.
>
> Thank you soooo much!I DONT THINK , cause for some reason no one ever replies to my posts. Maybe i am invisible. Im getting very frustrated because it seems any site i look at no or anyone i ask no one will reply. Argh!
Posted by Wildflower on September 25, 2003, at 13:17:11
In reply to No it doesnt exist, posted by Michelle0202 on September 25, 2003, at 13:08:44
I DONT THINK , cause for some reason no one ever replies to my posts. Maybe i am invisible. Im getting very frustrated because it seems any site i look at no or anyone i ask no one will reply. Argh!
I understand you frustration with posting. You're not invisible to me... :-)
Posted by DSCH on September 25, 2003, at 13:32:42
In reply to No it doesnt exist, posted by Michelle0202 on September 25, 2003, at 13:08:44
> > I'm still pretty new to this board and I'm honestly frustrated that I can't understand some of the medical posts.
> >
> > Is there a website that I can refer to that would explain the difference between MAOIs, SSRIs, mood stabilizers and anxiety meds and also provide me with prescription names? I'm going back to my pdoc in a few weeks and I want to be armed with knowledge regarding possible treatment options for my depression and SAD.
> >
> > Thank you soooo much!
>
> I DONT THINK , cause for some reason no one ever replies to my posts. Maybe i am invisible. Im getting very frustrated because it seems any site i look at no or anyone i ask no one will reply. Argh!I am worrking on a BIG post at the moment that will basically be something like a "Beginner's Guide to Psychopharmacology" from the standpoint of a "somewhat educated non-professional" (i.e ME). Have patience, I will have it ready later this afternoon. I need FOOD at the moment! :-)
Posted by Wildflower on September 25, 2003, at 13:50:17
In reply to Re: No it doesnt exist, posted by DSCH on September 25, 2003, at 13:32:42
> I am worrking on a BIG post at the moment that will basically be something like a "Beginner's Guide to Psychopharmacology" from the standpoint of a "somewhat educated non-professional" (i.e ME). Have patience, I will have it ready later this afternoon. I need FOOD at the moment! :-)
>Thank you! That sounds wonderful! I'll keep checking back for it.
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.
Posted by djmmm on September 25, 2003, at 15:38:33
In reply to Does this site exist?, posted by Wildflower on September 25, 2003, at 11:28:13
> I'm still pretty new to this board and I'm honestly frustrated that I can't understand some of the medical posts.
>
> Is there a website that I can refer to that would explain the difference between MAOIs, SSRIs, mood stabilizers and anxiety meds and also provide me with prescription names? I'm going back to my pdoc in a few weeks and I want to be armed with knowledge regarding possible treatment options for my depression and SAD.
>
> Thank you soooo much!Yes..there are plenty of sites...
http://www.mentalhealth.com/
http://www.neuropharmacology.com/
http://www.preskorn.com/books/ssri_s4.html
http://www.vh.org/cgi-bin/htsearch?words=maoi&config=vh&restrict=
http://www.neuro.jhmi.edu/Epilepsy/meds/
http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202084.html
Posted by Wildflower on September 26, 2003, at 10:10:55
In reply to A Beginner's Guide to Psychopharmacology, posted by DSCH on September 25, 2003, at 15:31:58
Posted by Been-There on September 26, 2003, at 12:19:48
In reply to No it doesnt exist, posted by Michelle0202 on September 25, 2003, at 13:08:44
<I DONT THINK , cause for some reason no one ever replies to my posts. Maybe i am invisible. Im getting very frustrated because it seems any site i look at no or anyone i ask no one will reply. Argh! >
It's easy to feel that way on busy message boards, especially when you have low self esteem like most of us do who come here. I think the real problem is that there is just too many messages to sift through and not enough time to read and answer them all.
I used to moderate a busy board like this and it was really tough keeping up with all the posts and there were like three of us trying to sift through them to delete, edit, and read. It was very time consuming to keep up with.
Posted by Tabitha on September 26, 2003, at 18:39:22
In reply to A Beginner's Guide to Psychopharmacology, posted by DSCH on September 25, 2003, at 15:31:58
Posted by DSCH on September 26, 2003, at 23:18:43
In reply to A Beginner's Guide to Psychopharmacology, posted by DSCH on September 25, 2003, at 15:31:58
If there is anything in this post that is unclear or wrong, please let me know by posting in this thread.
I think the difference between irreversible vs. reversible oxidation inhibition could use a little more explanation (as my recollection of that is unclear anyway!). Other than that I am pleased with how it turned out.
Posted by HenryO on September 27, 2003, at 1:37:15
In reply to Re: A Beginner's Guide to Psychopharmacology, posted by DSCH on September 26, 2003, at 23:18:43
Nice work, you deserve to be proud. Thank you
Posted by djmmm on September 27, 2003, at 10:36:17
In reply to Re: A Beginner's Guide to Psychopharmacology, posted by DSCH on September 26, 2003, at 23:18:43
> If there is anything in this post that is unclear or wrong, please let me know by posting in this thread.
>
> I think the difference between irreversible vs. reversible oxidation inhibition could use a little more explanation (as my recollection of that is unclear anyway!). Other than that I am pleased with how it turned out.try this thread: http://www.dr-bob.org/babble/20020402/msgs/101452.html
Posted by DSCH on September 27, 2003, at 17:38:14
In reply to Re: A Beginner's Guide to Psychopharmacology, posted by djmmm on September 27, 2003, at 10:36:17
> > If there is anything in this post that is unclear or wrong, please let me know by posting in this thread.
> >
> > I think the difference between irreversible vs. reversible oxidation inhibition could use a little more explanation (as my recollection of that is unclear anyway!). Other than that I am pleased with how it turned out.
>
> try this thread: http://www.dr-bob.org/babble/20020402/msgs/101452.htmlThanks, djmmm.
Right now I can see other problems with the MAOI/RIMA section.
I will make a post directly quoting from the relevant section of Perrine's book sometime tomorrow. It's not an easy read, but then these drugs are particularly hard to describe well in simple terms.
Posted by DSCH on September 30, 2003, at 0:32:08
In reply to Guide Errata: MAOI/RIMA, corrections soon, posted by DSCH on September 27, 2003, at 17:38:14
Source:
Perrine, Daniel M.
"The Chemistry of Mind-Altering Drugs: History, Pharmacology, and Cultural Context"
American Chemical Society, 1996, p. 233-5.[Note: Brofaromine appears to have been dropped just short of marketing by Ciba-Geigy]
Monoamine Oxidase Inhibitors.
Discovery. Monoamine Oxidase (MAO) inhibitors (MAOI) were discovered by accident during clinical trials of the antitubercular drug iproniazid during the 1950s. Isolated from family, friends, and their ordinary occupations and confronted with a life-threatening disease, many of the patients in the tuberculosis sanatoria of the day were understandably depressed [40], and it was soon noticed at several centers that the mood of those patients taking the antitubercular drug iproniazid was improved. It was hypothesized that iproniazid had an antidepressant effect because it blocks the enzyme MAO, which metabolizes excess epinepherine and serotonin (see Chapter 1) within the presynapse. Inhibiting the action of this enzyme would make more epinepherine and serotonin available.
Mode of Action. These early MAOIs are all "suicide substrate" irreversible inhibitors of MAO, a flavin-containing enzyme found in the mitochondria of neurons, intestinal mucosa, the liver, etc. Iproniazid contains a hydrazine (-NHNH2) function that is oxidized by MAO to a reactive intermediate that binds irreversibly to the flavin prosthetic group of the enzyme, rendering it inactive. Maximal inhibition of MAO activity is usually achieved in a few days (although, as with all antidepressants, psychological effects are not seen for 2-3 weeks), and after medication is discontinued, it requires 1-2 weeks for MAO activity to be restored to normal.
Side Effects. Iproniazid was replaced with better MAOIs, but all MAOIs still share common awkward side effects: orthostatic hypotension, sexual dysfunction (impotence, delayed ejaculation, loss of libido), and an unusual food/drug interaction: any foods or beverages containing large amounts of tyramine can cause a hypertensive crisis (headache, tachycardia, nausea and occasionally subarachnoid hemorrage). Foods containing tyramine are aged cheeses, wines, beers, dried meats and fish, and fava beans. The tyramine (4-hydroxyphenethylamine, also called tyrosamine) in these foods does not normally affect us because it is rapidly converted by MAO in the intestines to tyrosine, a common amino acid; absent this protective mechanism, tyramine enters the storage vessels for norepinepherine (NE) and displaces the NE, causing a drastic rise in blood pressure.
Phenelzine, Isocarboxazid, and Tranylcypromine. Phenelzine (Nardil, 5-30, Figure 5.7), isocarboxazid (Marplan, 5-31), and Tranylcypromine (Parnate, 5-32), are all used for clinical depression, panic disorder, and phobic disorders. Phenelzine, developed by Warner-Lambert, represents a simple substitution of hydrazine for the amine function of phenethylamine. Phenelzine also may improve eating behavior in some bulimics, but controlled clinical trials have not yet confirmed this. Isocarboxazid is an elaboration of the phenelzine structure, and is probably converted to it in vivo. Tranylcypromine can be seen either as a modification of phenethylamine or as an amphetamine with the side chain cyclized into a cyclopropane ring; in larger doses than those used to treat depression, it can cause psychomotor stimulation, and the development of dependence occasionally has been reported.
Reversible Inhibitors of Monoamine Oxidase A.
More recent research shows that there are two types of MAO enzyme, MAOA and MAOB. Whereas MAOB is more active in the peripheral system and metabolizes dietary tyramine, it is the inhibition of MAOA enzyme in the CNS that is responsible for the antidepressant efficacy of the MAOIs [41]. Older drugs such as phenelzine, isocarboxazid, and tranylcypromine irreversibly inhibit both enzyme types, but some newer drugs used in Europe are selective for MAOA. These reversible inhibitors of MAOA (RIMAs) are active antidepressants but do not induce a "cheese effect" hypertensive crisis if tyramine-containing foods are eaten.
Moclobemide. Moclobemide (Aurorix, 5-33, Figure 5.8) was first marketed by Hoffman-LaRoche in Sweden in 1990,and was subsequently approved for marketing in about 50 countries. It was the first of the RIMA class of drugs, and it shows good promise. In a randomized multicenter study comparing its efficacy to that of tranylcypromine, moclobemide was equally efficacious but had the clear advantage of a safer profile and slightly better tolerability [42]. However, studies from the Danish University Antidepressant Group have indicated that moclobemide, citalopram, and paroxetine are all somewhat less effective than clomipramine [43]. In a comparitive study of moclobemide and fluoxetine, tolerance of both drugs was quite good and efficacy statistically identical; whereas sedation, nausea, and vomiting were reported more frequently with fluoxetine, insomnia was more common with moclobemide [44].
Brofaromine, 5-34. In a randomized, double-blind Canadian study, this new RIMA drug was compared to clomipramine in patients with panic disorder with or without agoraphobia [45]. The drugs proved to be of equal efficacy, and the much more favorable safety and reduced side effects of the RIMA will most likely make it prefferable to clomipramine. In a review of trials using brofaromine for patients with major depression who did not respond to current antidepressant medications, brofaromine was judged equally effective but better tolerated and safer to use [46].
References and Notes.
40. Thomas Mann's The Magic Mountain provides an unforgettable impression of the psychological atmosphere prevading these institutions.
41. It is perhaps the reversability of the newer MAO agents rather than the selectivity that leads to their improved profile: the predominant enzyme active in metabolizing tyramine in the human intestine is MAO-A: Anderson, M.C.; Hasan, F,; et al. "Monoamine oxidase inhibitors and the cheese effect," Neurochem. Res., 1993, 18, 1145-1149.
42. Heinze, G.; Rossel, L. et al., "Double-blind comparison of moclobemide and tranylcypromine in depression," Pharmacopsychiatry, 1993, 26, 240-245.
43. (a) Vestergard, P.; Gram, L.F.; et al., "Therapeutic potentials of recently introduced antidepressants," Psychopharmacol. Ser., 1993, 10, 190-198. (b) Danish University Antidepressant Group, "Moclobemide a reversible MAO-A inhibitor showing weaker antidepressant effect than clomipramine in a controlled multicenter study," J. Affect. Disord., 1993, 28, 105-116.
44. Williams, R; Edwards, R.A.; et al., "A double-blind comparison of moclobemide and fluoxetine in the treatment of depressive disorders," Int. Clin. Psychopharmacol., 1993, 7, 155-158.
45. Bakish, D.; Saxena, B.M.; et al., "Reversible monoamine oxidase-A inhibitors in panic disorder," Clin. Neuropharmacol., 1993, 16, Suppl. 2, S77-S82.
46. Nolen, W.A.; Hoencamp, E; et al., "Reversible monoamine oxidase-A inhibitors in resistant major depression," Clin. Neuropharmacol., 1993, 16, Suppl. 2, S69-S76.
Posted by fabbabble on October 27, 2008, at 14:36:50
In reply to A Beginner's Guide to Psychopharmacology, posted by DSCH on September 25, 2003, at 15:31:58
The link referred to below can be accessed at the web archive site:
http://web.archive.org/web/20030810024533/http://www.nutritional-healing.com.au/neurotransmitters.htm
> 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.
>
Posted by fabbabble on October 27, 2008, at 14:38:06
In reply to Does this site exist?, posted by Wildflower on September 25, 2003, at 11:28:13
YES, check out http://web.archive.org/web/20030810024533/http://www.nutritional-healing.com.au/neurotransmitters.htm
RE:
> I'm still pretty new to this board and I'm honestly frustrated that I can't understand some of the medical posts.
>
> Is there a website that I can refer to that would explain the difference between MAOIs, SSRIs, mood stabilizers and anxiety meds and also provide me with prescription names? I'm going back to my pdoc in a few weeks and I want to be armed with knowledge regarding possible treatment options for my depression and SAD.
>
> Thank you soooo much!
Posted by fabbabble on October 27, 2008, at 14:48:51
In reply to Re: No it doesnt exist » DSCH, posted by Wildflower on September 25, 2003, at 13:50:17
Here are links to both sites mentioned in the article:
AND
This is the end of the thread.
Psycho-Babble Medication | Extras | FAQ
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.org
Script revised: February 4, 2008
URL: http://www.dr-bob.org/cgi-bin/pb/mget.pl
Copyright 2006-17 Robert Hsiung.
Owned and operated by Dr. Bob LLC and not the University of Chicago.