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dc.contributor.author
Beck, Paige
dc.contributor.author
Urbano Suarez, Francisco Jose
dc.contributor.author
Williams, D. Keith
dc.contributor.author
Garcia Rill, Edgar
dc.date.available
2017-07-11T19:13:51Z
dc.date.issued
2013-07
dc.identifier.citation
Beck, Paige; Urbano Suarez, Francisco Jose; Williams, D. Keith; Garcia Rill, Edgar; Effects of leptin on pedunculopontine nucleus (PPN) neurons; Springer Wien; Journal Of Neural Transmission. General Section.; 120; 7; 7-2013; 1027-1038
dc.identifier.issn
0300-9564
dc.identifier.uri
http://hdl.handle.net/11336/20140
dc.description.abstract
Leptin, a hormone that regulates appetite and energy expenditure, is increased in obese individuals, although these individuals often exhibit leptin resistance. Obesity is characterized by sleep/wake disturbances, such as excessive daytime sleepiness, increased REM sleep, increased nighttime arousals, and decreased percentage of total sleep time. Several studies have shown that short sleep duration is highly correlated with decreased leptin levels in both animal and human models. Arousal and rapid eye movement (REM) sleep are regulated by the cholinergic arm of the reticular activating system, the pedunculopontine nucleus (PPN). The goal of this project was to determine the role of leptin in the PPN, and thus in obesity-related sleep disorders. Whole-cell patch-clamp recordings were conducted on PPN neurons in 9- to 17-day-old rat brainstem slices. Leptin decreased action potential (AP) amplitude, AP frequency, and h-current (IH). These findings suggest that leptin causes a blockade of Na+ channels. Therefore, we conducted an experiment to test the effects of leptin on Na+ conductance. To determine the average voltage dependence of this conductance, results from each cell were equally weighted by expressing conductance as a fraction of the maximum conductance in each cell. INa amplitude was decreased in a dose-dependent manner, suggesting a direct effect of leptin on these channels. The average decrease in Na+ conductance by leptin was ~40 %. We hypothesize that leptin normally decreases activity in the PPN by reducing IH and INa currents, and that in states of leptin dysregulation (i.e., leptin resistance) this effect may be blunted, therefore causing increased arousal and REM sleep drive, and ultimately leading to sleep-related disorders.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Springer Wien
dc.rights
info:eu-repo/semantics/restrictedAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Leptin
dc.subject
Sodium Channels
dc.subject
H-Current
dc.subject
Brainstem
dc.subject
Pedunculopontine Nucleus
dc.subject.classification
Neurociencias
dc.subject.classification
Medicina Básica
dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Effects of leptin on pedunculopontine nucleus (PPN) neurons
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2017-07-11T13:25:19Z
dc.identifier.eissn
1435-1463
dc.journal.volume
120
dc.journal.number
7
dc.journal.pagination
1027-1038
dc.journal.pais
Austria
dc.journal.ciudad
Viena
dc.description.fil
Fil: Beck, Paige. University Of Arkansas For Medical Sciences; Estados Unidos
dc.description.fil
Fil: Urbano Suarez, Francisco Jose. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Fisiología, Biología Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Fisiología, Biología Molecular y Neurociencias; Argentina
dc.description.fil
Fil: Williams, D. Keith. University Of Arkansas For Medical Sciences; Estados Unidos
dc.description.fil
Fil: Garcia Rill, Edgar. University Of Arkansas For Medical Sciences; Estados Unidos
dc.journal.title
Journal Of Neural Transmission. General Section.
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1007/s00702-012-0957-x
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs00702-012-0957-x


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