Posted by AndrewB on April 26, 2000, at 11:07:18
In reply to Re:Down-Regulation and Tolerance: Qs for PeterJ, posted by PeterJ on April 26, 2000, at 1:46:17
Peter,
Thank you very much for your answers to my questions. They werre better answers than I could have hoped for. I am truly grateful for the opportunity to ‘talk’ with someone as informed as you are. I am fascinated about issues concerning dopamine potentiation , especially D2-D3 potentiation. I hope you will be able to answer these further questions. I have limited my questions to just those that are important to my condition at this time.
1) Are there rough equivalents to amineptine. For example, are COMT inhibitors possibly substitutes since they would result in increased dopamine in the synaptic clefts as does amineptine. By the way, does it seem like COMT inhibitors have AD potential either alone or in combo with an MAO-A, MAO-I or L-Dopa.
2) Can tyrosine supplementation potentiate the effect of amineptine. One person stated that tyrosine potentiated dexadrine by preventing dopamine depletion. Amphetamines like dexadrine are D2 reuptake blockers. Amineptine has similar mechanics, being a dopamine reuptake blocker.
3) Is it important to use a dopamine neuron neuroprotective agent such as pramipexole (a D2 agonist) when using agents such as amineptine that raise dopamine levels. Pramipexole may provide its neuroprotective effects through the depression of dopamine metabolism, antioxidant effects and the stimulation of trophic activity.
4) Is it possible for exercise to deplete dopamine and NE stores. After hard exercise, when unmedicated, I experience extreme mental fatigue following exercise. It starts maybe 12 hours (the next morning) after the exercise and lasts for maybe three days after that. Symptoms include loss of memory, mental confusion, busy head (increased internal dialogue, often self critical), lack of vigilance, physical fatigue, irritability, dysphoria, feelings of vulnerability, feelings of indecision, tiredness, spots and worms (floaters) in visual field sometimes accompanied by vertigo and mild orthostatic hypotension. It can get so bad that I’m not able to remember my own phone number or do simple number tasks. NE and dopamine (especially D2,D3) receptor transmission enhancers such as amisulpride and reboxetine are able to completely take away these symptoms except for the muscle soreness. The muscle soreness is taken away by high doses of 7-keto DHEA.
5) Does D1 receptor stimulation potentiate D2 receptor function. Does serotonin potentiate D2 receptor function. There is apparently a complex interrelationship of potentiation and inhibition between different dopamine receptors. Also, it is thought that part of the AD effect of serotenergic ADs is due to enhancement of D2 function.
Sorry to ask so many questions. They all however are so important to me.
Sincerely,
AndrewB
poster:AndrewB
thread:30864
URL: http://www.dr-bob.org/babble/20000420/msgs/31334.html