Posted by bleauberry on February 6, 2010, at 16:10:51 [reposted on February 22, 2010, at 1:20:57 | original URL]
In reply to Re: Dopamine not the magic answer folks, posted by linkadge on February 6, 2010, at 10:26:44
Just to casually jump in the conversation, I share Link's views on this topic. Brain chemistry is so much more complicated. One neurotransmitter cannot be impacted without also causing downstream impacts on all the others, secondary messengers, enzymes, and genetic coding. Also, the region of the brain in which the drug targets will contribute to the outcome. Most meds are region specific, a region that may or may not be involved in that person's symptoms, a region that may worsen symptoms, or a region that will cause untoward side effects.
Anhedonia can be relieved with serotonin meds. NE meds. DA meds. Gaba meds. Antipsychotics. Stimulants. We often think anhedonia is a hypo-dopamine thing, but what about the person who has get-up-and-go on Xanax, or the person who becomes alive again on Prozac or Lexapro?
Trying to correct a "supposed" dopamine deficiency can result in psychosis, fear, agitation, and depression. Indeed, longterm dopamine stimulators usually end in depression.
Cocaine gets much of it's action from the serotonin system.
In reality, it is a complex interplay of all the neurotransmitters and their receptors, not any single one.
It's just aint that easy. More complicated than we will ever know in our lifetimes.
The only real way to find out what does what for a particular person, is to try it and see what happens.
Back to the start of this thread, if they are looking for a balanced antidepressant with potential to help even someone who failed ECT, it's already here. Describing the mechanism of that antidepressant or any other however is rather futile, except in terms of predicting common side effects.
Personal trial is all that matters. Someone can find the absolute best thing on paper for their symptoms, and it turns out to be a drug from hell. Ya just can't predict.
> I don't know where this whole idea of dopamine being the magic cure comes from. So many people come on this board and say "I've got a dopamine problem because I have yadi-yada symptoms".
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> Fist off, there are virtually no AD's that target dopamine. Wellbutrin (contrary to popular belief) has only very weak effects on the dopamine transporter.
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> Mirapex is also not a miracle antidepressant.
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> Animals studies also show that if you increase dopamine in the pleasure centres of the brain it activates BDNF in that area. BDNF in the neucleus accumbens produces behavioral depression.
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> Long term admistration of many drugs of abuse often increases feelings of craving and of depression.
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> You can block the behavioral depressant effects of accumbal dopamine by administering antipsychotics. This is why antipsychotics probably have a better record of being adjuncts for depression than do stimulants.
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> D3 receptor activation likely produces the depressant effects as mice lacking the d3 receptor do not respond this way to dopaminergic drugs.
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> Infact mice that have been administered dopamine precursors or dopaminergic drugs behave like they have been defeated in social models of depression. Serotonin on the other hand facilitates social dominance.
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> There is a difference between pleasure and an antidepressant effect. For instance, smoking weed. Sure you get a hit, then you just feel like a looser.
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> Linkadge
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poster:bleauberry
thread:937616
URL: http://www.dr-bob.org/babble/neuro/20091104/msgs/937619.html