Chronic electroconvulsive treatment increases the activity of nitric oxide synthase in the rat brain.

Activation of the NMDA receptor complex increases the intracellular free Ca2+ concentration, which in turn influences a nitric oxide synthase (NOS) activity. In this study we investigated the NOS activity after acute and chronic electroconvulsive treatment in different rat brain regions. Chronic (10 daily treatments) but not acute (single treatment) significantly increased the NOS activity by 60% in the cerebral cortex and by 20-30% in hippocampus and cerebellum. The increased NOS activity might be a compensatory mechanism which balanced the reduced NMDA receptor complex reactivity. In fact, the adaptation of the NMDA receptor complex induced by chronic electroconvulsive treatment (and antidepressant drugs) measured at the receptor level, suggests the subsensitivity of that complex. Present results support the hypothesis of the critical role of the NMDA receptor pathway in the mechanism of antidepressant action.