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Effects of Chronic REM Sleep Restriction on D(1) Receptor and Related Signal Pathways in Rat Prefrontal Cortex

The prefrontal cortex (PFC) mediates cognitive function that is sensitive to disruption by sleep loss, and molecular mechanisms regulating neural dysfunction induced by chronic sleep restriction (CSR), particularly in the PFC, have yet to be completely understood. The aim of the present study was to...

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Detalles Bibliográficos
Autores principales: Han, Yan, Wen, Xiaosa, Rong, Fei, Chen, Xinmin, Ouyang, Ruying, Wu, Shuai, Nian, Hua, Ma, Wenling
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4352426/
https://www.ncbi.nlm.nih.gov/pubmed/25793215
http://dx.doi.org/10.1155/2015/978236
Descripción
Sumario:The prefrontal cortex (PFC) mediates cognitive function that is sensitive to disruption by sleep loss, and molecular mechanisms regulating neural dysfunction induced by chronic sleep restriction (CSR), particularly in the PFC, have yet to be completely understood. The aim of the present study was to investigate the effect of chronic REM sleep restriction (REM-CSR) on the D(1) receptor (D(1)R) and key molecules in D(1)R' signal pathways in PFC. We employed the modified multiple platform method to create the REM-CSR rat model. The ultrastructure of PFC was observed by electron microscopy. HPLC was performed to measure the DA level in PFC. The expressions of genes and proteins of related molecules were assayed by real-time PCR and Western blot, respectively. The general state and morphology of PFC in rats were changed by CSR, and DA level and the expression of D(1)R in PFC were markedly decreased (P < 0.01, P < 0.05); the expression of phosphor-PKAcα was significantly lowered in CSR rats (P < 0.05). The present results suggested that the alteration of neuropathology and D(1)R expression in PFC may be associated with CSR induced cognitive dysfunction, and the PKA pathway of D(1)R may play an important role in the impairment of advanced neural function.