Thread: 5htp
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Old 12-12-2006, 05:01 PM
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mrsD mrsD is offline
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Join Date: Aug 2006
Location: Great Lakes
Posts: 33,508
15 yr Member
Lightbulb This is an interesting question...

Here is a really good article that explains some of the neurotransmitter
issues.

http://www.mcmanweb.com/article-236.htm

Of course, not everything is as simple as it can seem. Many neurotransmitters
have alternate effects on other ones. For example, high serotonin concentrations in the brain, tend to downreglulate dopamine over time, so
effects can be secondary.

Here is a quote from that website:
Quote:
Gerard Sanacora MD, PhD of Yale has used magnetic resonance spectroscopy to measure GABA in the brain, finding that those with melancholic depression show low GABA concentrations in the occipital cortex, while the depletion is not as pronounced for those with atypical depression, indicating a diagnostic potential for subtypes of depression (March, 2003 American Journal of Psychiatry). Before and after scans of eight patients who had ECT found a doubling of GABA, and similar scans of patients on SSRIs showed a slow rise in GABA levels in nine of 11 of them.
Typically SSRIs which raise serotonin in the synapse are used to treat anxiety. Some people do well on 5-HTP and others get agitated on it. Alot depends on dose.

Here is an interesting site explaining neurotransmitters...
https://www.neurorelief.com/index.ph...=149&Itemid=48
Quote:
Taurine is an inhibitory neurotransmitter involved in neuromodulatory and neuroprotective actions. Supplementing with taurine can have a specific effect on GABA function.There are two primary ways in which taurine affects GABA.; First, it can inhibit GABA transaminase, an enzyme that metabolizes GABA. This allows GABA to stay in the synaptic cleft longer to bind to the postsynaptic receptor. Second, taurine can bind to the GABAAreceptor mimicking the effects of GABA. By helping GABA function, taurine is an important neuromodulator for prevention of excitoxicity. Excitability occurs when glutamate binds to its receptor, in this case, the NMDA receptor. Once glutamate activates the NMDA receptor there is an increase in intracellular Ca++ causing depolarization or cell excitability. With glutamate release, there is also simultaneous GABA and taurine release. When the inhibitory neurotransmitters, GABA and taurine, activate the GABAA receptor, the result is an increase in intracellular Cl- ions. This results in hyperpolarization which reduces cell excitability. Thus, the overall effect of taurine supplementation is to support GABA function. The relevance of GABA support is to prevent overstimulation due to high levels of excitatory amino acids. Therefore, taurine and GABA constitute an important protective mechanism against excessive excitatory amino acids. Similarly, taurine is increased in response to the exposure of free radicals elucidating its neuroprotective actions. Exposure to free radicals increases glutamate excretion, further potentiation NMDA receptor activation. Taurine modulates this effect to prevent cell excitability by keeping the cell hyperpolarized. The supplementation of taurine can help alleviate some excitability issues associated with elevated excitatory amino acids as well as play a role in regulating the effect of free radicals.
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