Modulation of glycinergic synaptic transmission in the trigeminal and hypoglossal motor nuclei by the nitric oxide-cyclicGMP signaling pathway.

In a previous work we found that nitric oxide (NO) and cyclicGMP (cGMP) inhibit glutamatergic synaptic transmission in trigeminal motoneurons (MnV). Here we study the actions of the NO/cGMP signaling pathway on glycinergic synaptic transmission in trigeminal and hypoglossal motoneurons (MnXII) in brain stem slices of neonatal rats. Glycinergic inhibitory postsynaptic currents (IPSCs) were recorded in MnV by stimulation of the supratrigeminal nucleus (SuV) and in MnXII by stimulation of the nucleus of Roller.

Inhibition of excitatory synaptic transmission in the trigeminal motor nucleus by the nitric oxide-cyclic GMP signaling pathway.

Nitric oxide (NO) and cyclic GMP (cGMP) suppressed glutamatergic synaptic transmission to trigeminal motoneurons in brain stem slices of neonatal rats. Histological studies showed guanylate cyclase (GC) containing fibers in the trigeminal motor pool. Glutamatergic excitatory postsynaptic currents (EPSCs) were recorded from neonatal trigeminal motoneurons in response to stimulation of the supratrigeminal nucleus (SuV).

The possible additional role of the cystic fibrosis transmembrane regulator to motoneuron inhibition produced by glycine effects.

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.

Nitrergic ventro-medial medullary neurons activated during cholinergically induced active (rapid eye movement) sleep in the cat.

The rostral ventro-medial medullary reticular formation is a complex structure that is involved with a variety of motor functions. It contains glycinergic neurons that are activated during active (rapid eye movement (REM)) sleep (AS); these neurons appear to be responsible for the postsynaptic inhibition of motoneurons that occurs during this state. We have reported that neurons in this same region contain nitric oxide (NO) synthase and that they innervate brainstem motor pools.

Serotoninergic control of glycinergic inhibitory postsynaptic currents in rat hypoglossal motoneurons.

This report presents the results of a study of the frequency potentiation of inhibitory postsynaptic currents (IPSCs) in hypoglossal motoneurons and its modulation by serotonin. A release-site model of synaptic plasticity was used to characterize the frequency-related potentiation of evoked IPSCs. Data were obtained to determine if the frequency potentiation of IPSCs occurs as a consequence of a low baseline quantal content of evoked IPSCs using whole cell patch-clamp recordings from hypoglossal motoneurons in the neonatal rat brainstem slice preparation.