The postsynaptic inhibitory control of lumbar motoneurons during the atonia of active sleep: effect of strychnine on motoneuron properties.
نویسندگان
چکیده
The present study examined the effects of strychnine on the tonic hyperpolarization and the changes in membrane properties of lumbar motoneurons that occur during active sleep. To carry out these studies, intracellular recordings from lumbar motoneurons were combined with the juxtacellular microiontophoretic application of strychnine in chronic, undrugged, normally respiring cats. During active sleep, compared to quiet sleep, motoneurons that were not exposed to strychnine exhibited tonic hyperpolarization, a decrease in cell excitability, and an increase in membrane conductance; they were also bombarded by high-frequency, large-amplitude IPSPs. In conjunction with the juxtacellular application of strychnine, there was a marked reduction in the degree of hyperpolarization during active sleep; motoneuron excitability was no longer suppressed, and there was a reduction in the increase in membrane conductance. In addition, the large-amplitude IPSPs were blocked. These results identify glycine as the neurotransmitter responsible for the state-dependent changes in membrane properties and the hyperpolarization of motoneurons that takes place during active sleep.
منابع مشابه
Evidence that glycine mediates the postsynaptic potentials that inhibit lumbar motoneurons during the atonia of active sleep.
Postsynaptic inhibition of somatic motoneurons underlies the atonia of active sleep. This inhibitory control depends, in large measure, on the bombardment of motoneurons during active sleep by a unique class of large-amplitude inhibitory postsynaptic potentials (IPSPs). These potentials are present only during this behavioral state and have therefore been designated as active sleep-specific IPS...
متن کاملThe motor inhibitory system operating during active sleep is tonically suppressed by GABAergic mechanisms during other states.
The present study was undertaken to explore the neuronal mechanisms responsible for muscle atonia that occurs after the microinjection of bicuculline into the nucleus pontis oralis (NPO). Specifically, we wished to test the hypothesis that motoneurons are postsynaptically inhibited after the microinjection of bicuculline into the NPO and determine whether the inhibitory mechanisms are the same ...
متن کاملElectrophysiological properties of lumbar motoneurons in the alpha-chloralose-anesthetized cat during carbachol-induced motor inhibition.
The present study was undertaken 1) to examine the neuronal mechanisms responsible for the inhibition of spinal cord motoneurons that occurs in alpha-chloralose-anesthetized cats following the microinjection of carbachol into the nucleus pontis oralis (NPO), and 2) to determine whether the inhibitory mechanisms are the same as those that are responsible for the postsynaptic inhibition of motone...
متن کاملGlycinergic and GABA(A)-mediated inhibition of somatic motoneurons does not mediate rapid eye movement sleep motor atonia.
A hallmark of rapid eye movement (REM) sleep is a potent suppression of postural muscle tone. Motor control in REM sleep is unique because it is characterized by flurries of intermittent muscle twitches that punctuate muscle atonia. Because somatic motoneurons are bombarded by strychnine-sensitive IPSPs during REM sleep, it is assumed that glycinergic inhibition underlies REM atonia. However, i...
متن کاملAdventures and tribulations in the search for the mechanisms of the atonia of REM sleep.
1473 The Background Thirty years ago, the first report was published with intracel-lular recordings from motoneurons, trigeminal motoneurons, in chronically instrumented, behaving cats across the sleep-wake cycle. A major observation was that synaptic activity, both ex-citatory and inhibitory, declined during rapid eye movement (REM) sleep in association with the characteristic motoneu-ronal hy...
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ورودعنوان ژورنال:
- The Journal of neuroscience : the official journal of the Society for Neuroscience
دوره 11 9 شماره
صفحات -
تاریخ انتشار 1991