Anhedonia — great intro and review at Medscape.com
Medscape.com has a very nice article on anhedonia, which is described as “an inability to experience pleasure from normally pleasurable life events such as eating, exercise, and social or sexual interaction”. Here, we bring an excerpt from the article. All currently marketed antidepressants are thought to work via monoaminergic mechanisms. The two most prevalent mechanisms […]
Medscape.com has a very nice article on anhedonia, which is described as “an inability to experience pleasure from normally pleasurable life events such as eating, exercise, and social or sexual interaction”. Here, we bring an excerpt from the article.
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.