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BioMed Research International
Volume 2015, Article ID 978236, 9 pages
http://dx.doi.org/10.1155/2015/978236
Research Article

Effects of Chronic REM Sleep Restriction on D1 Receptor and Related Signal Pathways in Rat Prefrontal Cortex

1Department of Neurology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China
2Department of Environmental Hygiene, Second Military Medical University, Shanghai 200433, China
3Minhang District Center for Disease Control and Prevention, Shanghai 201101, China
4Shanghai Sanatorium for Naval Retired Cadres, Shanghai 200434, China
5Pharmaceutical Center of Yueyang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200433, China

Received 3 July 2014; Accepted 17 November 2014

Academic Editor: John J. Gildea

Copyright © 2015 Yan Han et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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 D1 receptor (D1R) and key molecules in D1R’ 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 D1R in PFC were markedly decreased (, ); the expression of phosphor-PKAcα was significantly lowered in CSR rats (). The present results suggested that the alteration of neuropathology and D1R expression in PFC may be associated with CSR induced cognitive dysfunction, and the PKA pathway of D1R may play an important role in the impairment of advanced neural function.