But in depression there are low amounts of seretonin and noradrenalin so why would we want to further block these receptors so that the 5-HT and NA we do have cannot even bind ?
But in depression there are low amounts of seretonin and noradrenalin so why would we want to further block these receptors so that the 5-HT and NA we do have cannot even bind ?
This is an interesting phenomenon. Having had a look at where antidepressants act on serotonergic receptors, I have found that most antidepressants are: 5-HT1A-receptor agonists (decrease cAMP) 5-HT2A-receptor antagonists (decrease IP3 / Ca2+) 5-HT2C-receptor antagonists (decrease IP3 / Ca2+) 5-HT6-receptor antagonists (decrease cAMP) 5-HT7-receptor antagonists (decrease cAMP).
This seems to suggest that a decrease in second messengers is what is necessary for antidepressant activity.
However, this undermines how other antidepressants such as MAOIs, SSRIs and SNRIs work, which aim to increase levels of serotonin - the resultant increase in serotonin in the synapse would presumably activate the 5-HT receptors.