fearing that s/he isgoing crazy, which may intensify into depressive symptoms

To date, the monoaminergic (i.e., serotonergic, noradrenergic, dopaminergic) systems in the brain have received the greatest attention in neurobiological studies of mood disorders. These systems project widely to limbic, striatal and prefrontal cortical neuronal circuits that are implicated in the behavioral and visceral manifestations of mood disorders (reviewed in 10–12).

Together, these observations suggest that monoaminergic systems do not represent a final common pathway regulating mood, but rather exert a modulatory influence (see 13 for review).

It is thus noteworthy that recent studies have shown that the chronic administration of antidepressants can increase synaptic AMPA GluR1 receptors (35, 36).

The rapid antidepressant effects of ketamine have been postulated to occur via AMPA-mediated synaptic potentiation of critical neural circuits (32, 33). Increasing preclinical and clinical evidence demonstrates that synaptic plasticity, a fundamental mechanism of neuronal adaptation, is altered in mood disorders (34).