Posted by shasling on January 20, 2006, at 11:09:45
In reply to Re: Which ADs increase DOPAMINE the most? » SLS, posted by linkadge on January 20, 2006, at 10:19:26
> All very good points. I think that the rate of MAOI induced psychosis is similar between both Nardil and Parnate, (if that is any indication of the overall increase in dopaminergic neurotransmission)
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> And yes, if parante is a stimulant, then it might contribute to dopamine depletion.
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> I don't know if any direct tests have been done to compare nardil and parnate in their ability to affect dopaminergic neurotransmission.
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> >How do people know that they need dopamine in >the first place?
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> That is a good question. I don't mean to cause any disrespect, but I don't understand how people come to the conclusion. I suppose it is usually because SSRI's don't work for them. Anhedonia is not strictly indicitive of abnormal dopamine signalling. It would not be a problem if it were a benign assumption.
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> Anhedonia is generally a symptom of all types of depression, and has been effectively treated by antidepressants of many different classes.
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> The MSS4 gene has been implicated in anhedonia. When rats are stressed, they become anhedonic, and MSS4 drops. Both SSRI's and TCAs increase the MSS4 gene in the hippocampus.
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> MSS4 is thought to controll the excitability of limbic circutry.
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> I personally think that anhedonia is a sign of atrophy to certain hippocampal regions, people who are anhedonic can't even remember what is/was pleasurable.
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> But you are very right. We tend to assume things based on the *presumed* biochemical actions of a drug.
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> Linkadge
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> Guys, the short answer for me is that it is a complete lack of volition that causes me to lean in that direction. As well as the fact that serotonin tx does absolutely nothing, noradren/norepi tx makes my body go and causes me to run around, electrically, almost frantically just doing things, but there's still something very much missing; and I'm doing things sort of because I have to at the mercy of the adrenaline. On the correct dopaminergic, however, I have more energy, but it isn't based simply on my body being driven. I have energy because I find interest in things. The change feels very much like what I imagine 'normal' must be, rather than electric, and I have a reasonable amount of volition, initiative and reward. During the small window when Abilify (which only affects dopamine) was working for me, I finally felt absolutely normal, calm, productive and capable of doing everyday things; and I took care of everyday things because I *wanted* to, not because I *had* to, as is the feeling on noradr/norepi. Unfortunately, it later made me crazy and I had to stop taking it but that is beside the point...That having been said, and really with all due respect because you all do some really informed and helpful posts, I am disappointed that anyone who doesn't know those of us who have identified dopamine as our probable issue (and really who knows us better than us?) would question and/or discount that. I mean, we've all had enough of that from doctors and family members, etc. and it is never helpful and always degrading to be discounted in that way. That was one thing I immediately noticed about this site was that one's credibility about one's own condition was assumed, and that was such a gift. I am surprised and disappointed to find that kind of thing here, which had previously seemed like an unconditionally safe place where my knowledge of me would not be discounted by someone who 'knew' better.
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>Suzie
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poster:shasling
thread:599864
URL: http://www.dr-bob.org/babble/20060115/msgs/601061.html