β-adrenergic Receptor Activity in the Hippocampal Dentate Gyrus Participates in Spatial Learning and Memory Impairment in Sleep-deprived Rats

被引:12
作者
Lu, Huan-Jun [1 ]
Lv, Jing [2 ]
机构
[1] Nantong Univ, Inst Pain Med & Special Environm Med, Nantong 226019, Jiangsu, Peoples R China
[2] Hebei Univ Engn, Dept Physiol, Handan 056000, Hebei, Peoples R China
关键词
beta-adrenoceptors; Hippocampal dentate gyrus; Sleep deprivation; Long-term potentiation; Spatial learning and memory; LONG-TERM POTENTIATION; LOCUS-COERULEUS; LTP; NOREPINEPHRINE; DEPRIVATION; MODULATION; TETANIZATION; ENHANCEMENT; INVOLVEMENT; SUBREGIONS;
D O I
10.5607/en20058
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Sleep deprivation (SD) leads to cognitive impairment, especially hippocampus-dependent learning and memory (L&M). The hippocampal dentate gyrus (DG) is the key structure involved in spatial L&M while long-term potentiation (LTP) is an important cellular mechanism responsible for L&M. Physiological and behavioral evidences support the hypothesis that norepinephrine (NE) and beta-adrenoceptors (beta-AR) may play an important role in regulating L&M, including LTP. However, it is enigmatic how beta-AR influences the LTP disruption or memory impairment under SD circumstances. In the present study, the rats were subjected to SD for 18 h per day for 21 consecutive days and cognitive capacity was assessed by the Morris water maze (MWM) test. We examined the extracellular concentration of NE in the DG using in vivo brain microdialysis and HPLC analysis. The amplitudes of field excitatory postsynaptic potential (fEPSP) were subsequently measured in the DG during MWM test in freely moving conscious rats. The extracellular concentrations of NE and fEPSP amplitudes in the DG were significantly increased during MWM test, while these responses were suppressed in SD rats. When fEPSP amplitudes in the DG were measured after local injection of isoproterenol (an agonist of beta-AR), SD rats significantly alleviated the fEPSP impairment and rescued deficits of spatial L&M. In addition, the reduced expression of N-methyl-Daspartate (NMDA) and a-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors in SD rats significantly increased by activation of beta-AR by isoproterenol in the DG. In conclusion, we propose that beta-adrenergic signaling can improve memory impairment in sleep-deficient rats by regulating synaptic efficiency and glutamatergic receptor expression.
引用
收藏
页码:144 / 154
页数:11
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