Intracellular analysis of synaptic mechanisms controlling trigeminal motoneuron activity during sleep and wakefulness.

Abstract

The chronic intracellular recording technique in unanesthetized cats was utilized to analyze the synaptic mechanisms functioning to control trigeminal jaw-closer motoneuron membrane activity during naturally occurring states of wakefulness, quiet sleep and active sleep. Antidromic spikes were blocked and their peak potential and absolute amplitude decreased during active sleep as compared to quiet sleep. There was a decrease in amplitude and an increase in rate of decay of the falling phase of the trigeminal Ia-induced monosynaptic excitatory postsynaptic potential (EPSP) during active sleep. Post-synaptic inhibition of jaw-closer motoneurons during active sleep may act to suppress somatic reflexes and produce muscular atonia. During rapid eye movement [REM] episodes of active sleep, as compared to active sleep without REM, there was a reduction in amplitude without any change in rate of decay of the monosynaptic EPSP. Presynaptic inhibitory processes may function to suppress somatic reflexes during REM episodes of active sleep. Based on comparisons with the inhibitory postsynaptic potential (IPSP) induced in jaw-closer motoneurons by inferior alveolar nerve stimulation, the inhibitory input to jaw-closer motoneurons during active sleep may be distributed predominantly onto dendritic compartments.