Literature DB >> 3666087

Behavioral state-specific inhibitory postsynaptic potentials impinge on cat lumbar motoneurons during active sleep.

F R Morales1, P Boxer, M H Chase.   

Abstract

High-gain intracellular records were obtained from lumbar motoneurons in intact, undrugged cats during naturally occurring states of wakefulness, quiet sleep, and active sleep. Spontaneous, discrete, inhibitory postsynaptic potentials (IPSPs) were found to impinge on lumbar motoneurons during all states of sleep and wakefulness. IPSPs which occurred during wakefulness and quiet sleep were of relatively low amplitude and had a low frequency of occurrence. During the state of active sleep there occurred a great increase in inhibitory input. This was the result of the appearance of large-amplitude IPSPs and of an increase in the frequency of low-amplitude IPSPs which were indistinguishable from those recorded during wakefulness and quiet sleep. In addition to a difference in amplitude, the time course of the large IPSPs recorded during active sleep further differentiated them from the smaller IPSPs recorded during wakefulness, quiet sleep, and active sleep; i.e., their rise-time and half-width were of longer duration and their rate-of-rise was significantly faster. We suggest that the large, active sleep-specific IPSPs reflect the activity of a group of inhibitory interneurons which are inactive during wakefulness and quiet sleep and which discharge during active sleep. These as yet unidentified interneurons would then serve as the last link in the brain stem-spinal cord inhibitory system which is responsible for producing muscle atonia during the state of active sleep.

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Mesh:

Year:  1987        PMID: 3666087     DOI: 10.1016/0014-4886(87)90252-4

Source DB:  PubMed          Journal:  Exp Neurol        ISSN: 0014-4886            Impact factor:   5.330


  15 in total

1.  GABAA receptor antagonism at the hypoglossal motor nucleus increases genioglossus muscle activity in NREM but not REM sleep.

Authors:  Janna L Morrison; Sandeep Sood; Hattie Liu; Eileen Park; Philip Nolan; Richard L Horner
Journal:  J Physiol       Date:  2003-02-28       Impact factor: 5.182

2.  Eye movements and abducens motoneuron behavior during cholinergically induced REM sleep.

Authors:  Javier Márquez-Ruiz; Miguel Escudero
Journal:  Sleep       Date:  2009-04       Impact factor: 5.849

3.  Glycine-mediated postsynaptic inhibition is responsible for REM sleep atonia.

Authors:  Peter J Soja
Journal:  Sleep       Date:  2008-11       Impact factor: 5.849

4.  Are all motoneurons created equal in the eyes of REM sleep and the mechanisms of muscle atonia?

Authors:  Gregory D Funk
Journal:  Sleep       Date:  2008-11       Impact factor: 5.849

5.  Confirmation of the consensus that glycinergic postsynaptic inhibition is responsible for the atonia of REM sleep.

Authors:  Michael H Chase
Journal:  Sleep       Date:  2008-11       Impact factor: 5.849

6.  Adventures and tribulations in the search for the mechanisms of the atonia of REM sleep.

Authors:  Leszek Kubin
Journal:  Sleep       Date:  2008-11       Impact factor: 5.849

7.  New pathways and data on rapid eye movement sleep behaviour disorder in a rat model.

Authors:  Kung-Chiao Hsieh; Darian Nguyen; Jerome M Siegel; Yuan-Yang Lai
Journal:  Sleep Med       Date:  2012-10-09       Impact factor: 3.492

8.  c-fos expression in brainstem premotor interneurons during cholinergically induced active sleep in the cat.

Authors:  F R Morales; S Sampogna; J Yamuy; M H Chase
Journal:  J Neurosci       Date:  1999-11-01       Impact factor: 6.167

9.  State-dependent control of lumbar motoneurons by the hypocretinergic system.

Authors:  Jack Yamuy; Simon J Fung; Mingchu Xi; Michael H Chase
Journal:  Exp Neurol       Date:  2009-12-03       Impact factor: 5.330

Review 10.  The anatomical, cellular and synaptic basis of motor atonia during rapid eye movement sleep.

Authors:  Elda Arrigoni; Michael C Chen; Patrick M Fuller
Journal:  J Physiol       Date:  2016-07-03       Impact factor: 5.182

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