krazyKemist
Critical Thinker
- Joined
- Jun 14, 2007
- Messages
- 430
Wait. This seems a bit tricky, but I'd like to understand it. When reuptake is inhibited, the increase in serotonin levels triggers a throttling back on natural serotonin production (similar to the way use of anabolic steroids leads to a decline in natural testosterone production). Plus, the body adapts to the increased serotonin levels in two other ways: a reduction in both the number of receptors and in their sensitivity. So when you stop, there is a deficiency, at least for a while. Right? So you're saying that the body adapts to that by increasing the number of receptors, but that natural production is never fully restored?
That's what this seems to indicate. If the serotonin levels are chronically low, the only way to normalize activity is increased sensitivity, ie either receptor modification (receptors may even become permanently activated, without need of ligand, but I don't think that's what's happening here) or higher number of receptors. And if sensitivity is higher, it would preclude increase in production, if the two are linked by cell signaling.
I'd say that for a while, higher than normal levels would be there because of overstocking thanks to the SSRI; then production would shut down, and serotonin stocks would go down. The increase in sensitivity may be linked to either low stocks or low circulating levels. If it's linked to stocks, the person may not experience a deficiency. It depends on the signaling.