Posted by NoMotic on December 16, 2003, at 12:06:16
In reply to Larry Hoover, can you weigh in on this? (nm), posted by psychlover on December 15, 2003, at 19:11:26
In my moderately educated opinion, I think that a higher level of dopamine does nothing but good for most depressives. I think obsessiveness comes from too little 5-HT, as evidenced by recent studies on OCD. Procrastination in my opinion comes from too little 5-HT and too little DA, a combo of both. I think most people know that caffeine makes one motivated... this is achieved presumably through indirect release of 5-HT, NE, and DA.
Increased 5-HT does not lead to lower DA, necessarily. Sometimes, yes, sometimes no. Increased activity in that 5-HT2a receptor decreases dopamine activity in the PFC. Increased activity at the 5-HT1a receptor increases dopamine activity. Note how newer antipsychotics achieve increases in PFC functioning through 5-HT1a agonism and 5-HT2a antagonism.
Thus, it is speculated that people who take SSRI's long term experience excessive stimulation of the 5-HT2a receptors on the DA nerve terminal which actually inhibits DA... and therefore antidepressant apathy appears.
I agree that a general state of high serotonin and high dopamine is most beneficial, but again this cannot apply across the board.
I think anxiety also involved too much epinephrine and norepinephrine in certain regions of the brain as well as too much serotonin in certain regions of the brain. Certain regions is the keyword here. Serotonin is activating in some respects, inhibiting in others.
Studies in monkeys show a U curve for norepinephrine - too little and one is underaroused. Too much and one is too aroused to block out external signals. Yet ADD is helped through increased norepinephrine in the synapse, thus increasing motivation and interest.
It's incredibly complex... obviously.
poster:NoMotic
thread:289601
URL: http://www.dr-bob.org/babble/alter/20031204/msgs/290542.html