Quinine, a selective gap junction blocker, decreases REM sleep in rats.

Electrical synapses are formed by gap junctions that allow the direct communication between neurons, the intercellular transference of ions and small molecules as well as the electrical coupling of the cells. Electrical coupling in neurons is mediated by the gap junction protein connexin36. There are reports about the presence of electrical coupling in the sublaterodorsal nucleus and pedunculopontine nucleus, which have been implicated in the modulation of the rapid eye movement sleep. In the present study, rats were used to examine the possible changes on the sleep-wake states after intracerebroventricular administration of several doses of quinine, a selective blocker of gap junctions formed by connexin36. The results showed that quinine significantly increased the time spent in wakefulness and decreased the time spent in slow wave sleep along the 24h of polygraphic recording. The three doses used of quinine caused a significant decrease of rapid eye movement sleep along the light phase; however, only one dose extended such effect until the darkness phase. The changes on sleep-wake states of the rat after the blockage of gap junctions formed by connexin36 suggest that electrical synapses could contribute to the regulation of sleep-wake states in concert with the well-known chemical neurotransmission.