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 β-adrenoceptors (β-AR) may play an important role in regulating L&M, including LTP. However, it is enigmatic how β-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 β-AR), SD rats significantly alleviated the fEPSP impairment and rescued deficits of spatial L&M. In addition, the reduced expression of N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors in SD rats significantly increased by activation of β-AR by isoproterenol in the DG. In conclusion, we propose that β-adrenergic signaling can improve memory impairment in sleep-deficient rats by regulating synaptic efficiency and glutamatergic receptor expression.

中文翻译：

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海马齿状回中的β-肾上腺素受体活性参与睡眠剥夺大鼠的空间学习和记忆障碍。

睡眠剥夺（SD）会导致认知障碍，尤其是海马依赖性学习和记忆（L＆M）。海马齿状回（DG）是参与空间L＆M的关键结构，而长期增强（LTP）是负责L＆M的重要细胞机制。生理和行为证据支持以下假设：去甲肾上腺素（NE）和β-肾上腺素能受体（β-AR）可能在调节L＆M（包括LTP）中起重要作用。然而，在SD情况下，β-AR如何影响LTP破坏或记忆障碍是令人费解的。在本研究中，大鼠连续21天每天接受SD刺激18小时，并通过莫里斯水迷宫（MWM）测试评估认知能力。我们使用体内方法检查了DG中NE的细胞外浓度脑微透析和HPLC分析。随后在自由移动的清醒大鼠的MWM测试期间，在DG中测量了场兴奋性突触后突触电位（fEPSP）的幅度。在MWM试验中，DG中NE和fEPSP振幅的细胞外浓度显着增加，而在SD大鼠中这些反应受到抑制。当局部注射异丙肾上腺素（β-AR的激动剂）后测量DG中的fEPSP振幅时，SD大鼠显着减轻了fEPSP损伤并挽救了空间L＆M的缺陷。此外，通过激活β-AR，SD大鼠的N-甲基-D-天冬氨酸（NMDA）和α-氨基-3-羟基-5-甲基异恶唑-4-丙酸（AMPA）受体表达降低。 DG中的异丙肾上腺素。综上所述，