Peng Jin, Huang Xinyu, Liu Peijie, Hu Yushi, Kang Liang
College of Sport Medicine and Health, Chengdu Sport University, Chengdu, 610041, China.
Institute of Sport Medicine and Health, Chengdu Sport University, Chengdu, 610041, China.
Purinergic Signal. 2025 Feb 19. doi: 10.1007/s11302-025-10072-z.
Adenosine, a sleep-associated neuromodulator, is crucial in various physiological and pathological processes. Previous studies have demonstrated that sleep deprivation (SD) alters striatal neuronal activity. In this study, we used in vitro electrophysiological recordings to investigate the effects of 20 h of SD on the neuronal excitability of mouse dorsal striatal medium spiny neurons (MSNs). Our findings revealed that SD resulted in altered action potential (AP) discharge properties and reduced neuronal excitability compared to the control group. Importantly, these changes were partially offset by the prophylactic injection of the A2A receptor (A2AR) antagonist SCH58261. Additionally, 20 h of SD caused a decrease in the amplitude and an increase in the interval of spontaneous excitatory postsynaptic currents (sEPSCs) compared to control. However, the prophylactic injection of the A2AR antagonism shortened the sEPSC interval, while the A1 receptor (A1R) antagonist DPCPX not only shortened the interval but also further reduced the amplitude of sEPSCs. Thus, it can be concluded that SCH58261 effectively prevents the reduction in excitability of striatal MSNs in mice following 20 h of sleep deprivation, whereas DPCPX does not.
腺苷是一种与睡眠相关的神经调节剂，在各种生理和病理过程中起着至关重要的作用。先前的研究表明，睡眠剥夺（SD）会改变纹状体神经元的活动。在本研究中，我们使用体外电生理记录来研究20小时的睡眠剥夺对小鼠背侧纹状体中等棘状神经元（MSNs）神经元兴奋性的影响。我们的研究结果显示，与对照组相比，睡眠剥夺导致动作电位（AP）发放特性改变，神经元兴奋性降低。重要的是，预防性注射A2A受体（A2AR）拮抗剂SCH58261可部分抵消这些变化。此外，与对照组相比，20小时的睡眠剥夺导致自发性兴奋性突触后电流（sEPSCs）的幅度降低，间隔增加。然而，预防性注射A2AR拮抗剂可缩短sEPSC间隔，而A1受体（A1R）拮抗剂DPCPX不仅缩短了间隔，还进一步降低了sEPSCs的幅度。因此，可以得出结论，SCH58261可有效防止小鼠在睡眠剥夺20小时后纹状体MSNs兴奋性的降低，而DPCPX则不能。
