Posted by linkadge on January 20, 2006, at 10:19:26
In reply to Re: Which ADs increase DOPAMINE the most? » linkadge, posted by SLS on January 20, 2006, at 6:57:53
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)
And yes, if parante is a stimulant, then it might contribute to dopamine depletion.
I don't know if any direct tests have been done to compare nardil and parnate in their ability to affect dopaminergic neurotransmission.
>How do people know that they need dopamine in >the first place?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.
Anhedonia is generally a symptom of all types of depression, and has been effectively treated by antidepressants of many different classes.
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.
MSS4 is thought to controll the excitability of limbic circutry.
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.
But you are very right. We tend to assume things based on the *presumed* biochemical actions of a drug.
Linkadge
poster:linkadge
thread:599864
URL: http://www.dr-bob.org/babble/20060115/msgs/601048.html