Literature DB >> 12207952

Intracellular recordings of pontine medial gigantocellular tegmental field neurons in the naturally sleeping cat: behavioral state-related activity and soma size difference in order of recruitment.

K Ito1, M Yanagihara, H Imon, L Dauphin, R W McCarley.   

Abstract

Intracellular recordings and neurobiotin labeling of medial pontine gigantocellular tegmental field (m-PFTG) neurons in the undrugged, naturally sleeping cat were performed to establish the relationship between soma size and membrane potential (MP) activity before and during the onset of the rapid eye movement (REM) phase of sleep. Initial recordings without labeling revealed that recorded neurons in the m-PFTG had a tonic, sustained membrane depolarization in REM sleep as compared with more polarized MP levels in slow-wave sleep (S) and phasic depolarizations in wakefulness (W) on a more polarized MP level. In neurobiotin-labeled neurons, there was a strong correlation between the soma size of m-PFTG neurons and the 'lead time', the time of onset relative to the beginning of REM, of a sustained increase in membrane depolarization. Thirty-nine m-PFTG neurons with soma cross-sectional areas ranging from 2098 microm(2) to 5958 microm(2) (mean value 3833.8 microm(2)) were analyzed. A majority of these m-PFTG neurons showed an increase in membrane depolarization associated with depolarizing postsynaptic potentials (PSPs) and spike generation that occurred before electrographic signs of REM sleep onset, while the rest of the neurons depolarized at the beginning of or just after REM sleep onset. Our previous work had suggested that many of these m-PFTG neurons were output neurons to the spinal cord. Analysis of the onset time of sustained membrane depolarization (Leadtime(MP)) revealed that larger cells had a longer lead time, while analysis of the lead times for onset of sustained PSPs and action potentials (Leadtime(AP)) showed this measure not to be dependent on soma size, but to be rather uniform, occurring just before the onset of REM sleep. Hence recruitment time, defined as the difference between Leadtime(AP) and Leadtime(MP), was dependent on cell soma size, implying that larger neurons may take longer to depolarize to an MP level critical for generating sustained action potentials, while smaller neurons may require less time. Copyright 2002 IBRO

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Year:  2002        PMID: 12207952     DOI: 10.1016/s0306-4522(02)00253-1

Source DB:  PubMed          Journal:  Neuroscience        ISSN: 0306-4522            Impact factor:   3.590


  5 in total

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

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

Review 3.  Control of sleep and wakefulness.

Authors:  Ritchie E Brown; Radhika Basheer; James T McKenna; Robert E Strecker; Robert W McCarley
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4.  Identification of cholinergic and non-cholinergic neurons in the pons expressing phosphorylated cyclic adenosine monophosphate response element-binding protein as a function of rapid eye movement sleep.

Authors:  S Datta; D F Siwek; E C Stack
Journal:  Neuroscience       Date:  2009-06-18       Impact factor: 3.590

5.  Why are seizures rare in rapid eye movement sleep? Review of the frequency of seizures in different sleep stages.

Authors:  Marcus Ng; Milena Pavlova
Journal:  Epilepsy Res Treat       Date:  2013-06-18
  5 in total

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