Alterations in the levels of monoamines in discrete brain regions of clomipramine-induced animal model of endogenous depression.

It has been hypothesized that the dysfunction of the serotonergic and catecholaminergic neurotransmission is involved in the pathogenesis of depression. These hypotheses are being tested in a novel rat model of depression developed by the treatment of antidepressant-clomipramine neonatally from postnatal day 8 to 21. After the attainment of adulthood, these rats mimicked the features of the human endogenous depression showing significant decrease in the aggressive behavior and food intake. Biogenic amine estimations in these rats revealed that the levels of serotonin and noradrenaline were decreased significantly (P < 0.001) in frontal cortex, hippocampus, brain stem, septum and hypothalamus, while the levels of dopamine were decreased significantly (P < 0.001) only in the hippocampus compared to normal control and vehicle treated groups of rats. Our results demonstrate the dysfunction of serotonergic and noradrenergic neurotransmission, with lesser involvement of dopaminergic neurotransmission in the clomipramine induced experimental model of depression.