The monoamine hypothesis postulates that the deficit of certain neurotransmitters is responsible for depression, and even that certain neurotransmitters are linked to specific symptoms.
If suppose serotonin deficit causes depression and antidepressants like TCAs causes increase in serotonin by decreasing uptake, it concludes to me that the increase in transmission via serotonergic receptors on post synaptic membrane alleviates depression.
My question is that how do antidepressants like atypical antidepressants more specifically Trazodone which acts as 5-HT2 antagonist show their antidepressant action? And TCAs also show such antagonism.
I believe the idea of increased serotonin to cause antidepressant action is not being satisfied here especially in this case of atypical antidepressant as the transmission is being blocked by serotonin receptor antagonistll.