共 29 条
Effects of Chronic REM Sleep Restriction on D1 Receptor and Related Signal Pathways in Rat Prefrontal Cortex
被引:3
作者:
Han, Yan
[1
]
Wen, Xiaosa
[2
,3
]
Rong, Fei
[2
]
Chen, Xinmin
[2
]
Ouyang, Ruying
[4
]
Wu, Shuai
[1
]
Nian, Hua
[5
]
Ma, Wenling
[2
]
机构:
[1] Second Mil Med Univ, Changhai Hosp, Dept Neurol, Shanghai 200433, Peoples R China
[2] Second Mil Med Univ, Dept Environm Hyg, Shanghai 200433, Peoples R China
[3] Minhang Dist Ctr Dis Control & Prevent, Shanghai 201101, Peoples R China
[4] Shanghai Sanat Naval Retired Cadres, Shanghai 200434, Peoples R China
[5] Shanghai Univ Tradit Chinese Med, Yueyang Hosp, Pharmaceut Ctr, Shanghai 200433, Peoples R China
基金:
中国国家自然科学基金;
关键词:
INTRINSIC EXCITABILITY;
SPATIAL MEMORY;
DEPRIVATION;
DOPAMINE;
MODULATION;
MECHANISMS;
D O I:
10.1155/2015/978236
中图分类号:
Q81 [生物工程学(生物技术)];
Q93 [微生物学];
学科分类号:
071005 ;
0836 ;
090102 ;
100705 ;
摘要:
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 (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 (P < 0.01, P < 0.05); the expression of phosphor-PKAc alpha was significantly lowered in CSR rats (P < 0.05). 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.
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