I think about this stuff a LOT, seeing as I am on Lexapro myself. Here is the basic theory I have on how SSRI type (and related medications work).
Many people report that SSRI medications ease their depressive symptoms, but also cause mood-deadening... I believe I understand why this is. When a person with depression is not on medication, their Serotonin levels are obviously untouched, and fluctuate from time to time around a homeostatic baseline. In this state, their are plenty of serotonin receptors avaliable for bonding to the neurotransmitter, so these changes are detected and handled in an optimum fashion.
With people who are currently depressed, these downward fluctuations may exasterbate (not cause) their depressive emotions. When a person begins an SSRI medication, the level of serotonin in the brain steadily rises for the first phase of the treatment, and then more-or-less plateuas. At this point, the brain attempts to achieve homeostasis once again, and does this by down-regulating it's serotonin receptors (as it does to other receptors when people abuse illegal drugs).
Once homeostasis is achieved, the brain now functions essentially the same way as it did before treatment, while having a higher level of serotonin. However, since the serotonin receptors have now down-regulated to adjust to the medication, the brains response to serotonin fluctuations will be "flattened"; Because there are less receptors, the brain should theoretically be less receptive of change at times where external (or internal) stimuli cause serotonin levels to change.
*Now, if this theory holds up (which I believe it does), you could potentially apply the same logic to a drug that inhibits the reuptake of norepinephrine or Dopamine. Assuming that a persons anxiety is at least somewhat caused by fluctuations of these neurotransmitters, one could potentially apply the same logic as above in an attempt to "flatline" the anxiety response. During the initial phase of treatment, anxiety could be greatly increased due to higher levels of one or both of these neurotransmitters... However, if one could ride the medication out for this initial adjustment period, it would make sense that the brain would re-regulate these receptors in a similar fasion as outlined above, and the fluctuations of the targetted neurotransmitters would be receptively reduced (directly coorelated to the level of inhibition).
Now, I don't know what the current theory is for depression (I know it's not a "serotonin imbalance"), but based on anecdotal reports I have read online, this makes perfect sense. This would explain why people have a difficult time during the startup of new medicatons, and why it takes a while for the medications true effects to shine. Based on my theory, these timelines would be directly coorelated to the rate at which an individuals brain is able to achieve homeostasis.
Thoughts? I am starting wellbutrin tommorow, and I am intrigued to see if my theory holds up in reality.
