Melatonin-induced inhibition of spinal cord synaptic potentiation in rats is MT2 receptor-dependent.

Systemically administered melatonin has been reported to produce antinociception and to inhibit spinal nociceptive transmission in rats. The present study was designed to investigate in anesthetized rats (i) whether intrathecally administered melatonin can depress synaptic potentiation (wind-up) in the spinal cord, and (ii) whether this effect is prevented by intrathecal (i.t.) administration of the MT2 receptor antagonist luzindole. Results showed that melatonin i.t. (10, 30 and 90 microg) induced dose-dependent inhibition of wind-up activity (ED50=52.06 microg i.t.), an effect that was prevented by 100 microg i.t. of luzindole. Since wind-up is dependent on NMDA receptor activation, the results suggest that melatonin can interfere with the NMDA-mediated glutamatergic component of pain transmission in rat spinal cord by acting on MT2 receptors.