5 - 4 - 43. Major Depression. Mechanisms of antidepressant action (10-10)

5 - 4 - 43. Major Depression. Mechanisms of antidepressant action (10-10)

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We're beginning now to synthesize everything that we've learned in this course about drug action and about the natural physiology of cells and neuroscience. And we're trying to put together a coherent story, if we can, about how antidepressants act. We'll take too many lectures to do this. How does the interaction between SSRIs and SERT relieve depression? Well, most experts would restate this question. How does blockade of serotonin re-uptake relieve depression via the presumed outside in mechanisms. In miniLecture 21, for instance, we've recapitulated the outside in pathways for gene activation downstream from g protein coupled receptors. There is also a serotonin-activated channel, the 5HT3 receptor. And in discussions about nicotine action and nicotine addiction we've said that. Some ligand-gated channels are permeable to calcium. This could start second messenger pathways, either directly or indirectly. This seems unlikely for the 5-HT3 receptor. It's not very calcium permeable. But let's keep that in mind. So, in general, then, the possible downstream consequences of changed regulation of serotenergic systems would be short term derangement of the modulation of synaptic strength. And possibly also, neuronal intrinsic properties. How keeping this going for two to three weeks, produces the faux effects of SSRI is not known. And then there's the possibility that these changes in intracellular function could lead to long-term changes in neuronal gene expression. How these might take two to the three, to three weeks is also not known, but the possibility exists. And there is also additional evidence for the action of serotonin and as we'll see
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