26 augustus 2007

Neuroscience Institute on Medscape

Interesting stuff on depression, insomnia , anhedonia.....etc.
Anhedonia as a Preclinical Model for Major Depression Gary Evoniuk, Ph.D. GSK Research & Development All currently marketed antidepressants are thought to work via monoaminergic mechanisms. The two most prevalent mechanisms are the blockade of serotonin, noradrenaline and/or dopamine reuptake (e.g. SSRIs, SNRIs, NDRIs) or the inhibition of monoamine break-down in the synaptic cleft via MAO inhibition. This led to the formulation of the monoamine hypothesis of depression, which suggests that depression arises from a deficiency in monoamine neurotransmission in brain areas critical to the regulation of mood and other key symptoms of the disorder. This theory continues to prevail, even in the absence of clear evidence of monoamine deficits in the brain of depressed humans or animals exhibiting depression-like behavior (Stahl SM. Essential Psychopharmacology. 2nd ed.), and has led to validation of current animal models of depression primarily on the basis of monaminergic mechanisms. Consequently, it is questionable whether these models would be useful in identifying effective antidepressant drugs that work via other mechanisms. It is interesting to note that the current lack of non-monoaminergic antidepressants cannot be attributed to lack of effort directed at their discovery and development, and major efforts to test other mechanisms (e.g. substance P antagonists, CRF antagonists, gonadal steroids) have yet to provide clear proof of efficacy in humans, and other potentially therapeutic mechanisms may remain untapped due to limitations of our current screening methods. Read more....

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