In the present work we study the contribution of the
chloride channel of the
Cystic Fibrosis Transmembrane Regulator (CFTR) in the postsynaptic inhibition of somatic motoneurons during rapid-eye-movement (REM) sleep atonia. Postsynaptic inhibition of motoneurons is partially responsible for the atonia that occurs during REM sleep. Disfacilitation is an additional mechanism that lowers motoneuron excitability in this state. Postsynaptic inhibition is mediated by the release of
glycine from synaptic terminals on motoneurons, and by
GABA that plays a complementary role to that of
glycine. In this work we look in brain stem motoneurons of neonatal rats at a mechanism unrelated to the actions of
glycine,
GABA or to disfacilitation which depends on the
chloride channel of the CFTR. We studied the presence of CFTR by immunocytochemistry. In electrophysiological experiments utilizing whole cell recordings in in vitro slices we examined the consequences of blocking this
chloride channel. The effects on motoneurons of the application of
glycine, of the application of
glibenclamide (a CFTR blocker) and again of
glycine during the effects of
glibenclamide were studied.
Glycine produced an hyperpolarization, a decrease in motoneuron excitability and a decrease in input resistance, all characteristic changes of the postsynaptic inhibition produced by this
neurotransmitter.
Glibenclamide produced an increase in input resistance and in motoneurons' repetitive discharge as well as a shift in the equilibrium potential for
chloride ions as indicated by the displacement of the reversal potential for glycinergic actions. In motoneurons treated with
glibenclamide,
glycine produced postsynaptic inhibition but this effect was smaller when compared to that elicited by
glycine in control conditions. The fact that blocking of the CFTR-
chloride channel in brain stem motoneurons influences glycinergic inhibition suggests that this channel may play a complementary role in the glycinergic inhibition that occurs during REM sleep.