School of Life Sciences, Jawaharlal Nehru University, New Delhi 110067, India.
Neurosci Lett. 2012 Jun 27;520(1):62-6. doi: 10.1016/j.neulet.2012.05.031. Epub 2012 May 17.
Rapid eye movement sleep (REMS) deprivation (REMSD) has been reported to elevate neurotransmitter level in the brain; however, intracellular mechanism of its increased release was not studied. Phosphorylation of synapsinI, a synaptic vesicle-associated protein, is involved in the regulation of neurotransmitter release. In this study, rats were REMS deprived by classical flowerpot method; free moving control (FMC), large platform control (LPC) and recovery control (REC) was carried out. In another set REMS deprived rats were intraperitoneally (i.p.) injected with α1-adrenoceptor antagonist, prazosin (PRZ). Effects of REMSD on Na-K ATPase activity and on the total synapsinI as well as phosphorylated synapsinI levels were estimated in synaptosomes prepared from whole brain. It was observed that REMSD significantly increased synaptosomal Na-K ATPase activity, which was prevented by PRZ. Western blotting of the same samples by anti-synapsinI and anti-synapsinI-phosphoSer603 showed that REMSD increased both the total as well as phospho-form of synapsinI as compared to respective levels in FMC and LPC samples. These findings suggest a functional link between REMSD and synaptic vesicular mobilization at the presynaptic terminal, a process that is essential for neurotransmitter release. The findings help explaining the intracellular mechanism of elevated neurotransmitter release associated to REMSD.
快速眼动睡眠 (REMS) 剥夺 (REMSD) 已被报道会提高大脑中的神经递质水平；然而，其释放增加的细胞内机制尚未得到研究。突触素 I 的磷酸化，一种与突触小泡相关的蛋白质，参与神经递质释放的调节。在这项研究中，大鼠通过经典花盆法被剥夺 REM；进行了自由移动对照 (FMC)、大平台对照 (LPC) 和恢复对照 (REC)。在另一组 REM 剥夺大鼠中，腹腔内 (i.p.) 注射了α1-肾上腺素受体拮抗剂，特拉唑嗪 (PRZ)。在从全脑制备的突触体中，评估了 REMSD 对 Na-K ATP 酶活性以及总突触素 I 和磷酸化突触素 I 水平的影响。结果表明，REMSD 显著增加了突触体 Na-K ATP 酶活性，而 PRZ 则阻止了这种增加。对相同样品进行抗突触素 I 和抗突触素 I-磷酸丝氨酸 603 的 Western 印迹显示，与 FMC 和 LPC 样品中的相应水平相比，REMSD 增加了总突触素 I 和磷酸化突触素 I 的水平。这些发现表明 REMSD 与突触小泡在突触前末端的动员之间存在功能联系，这是神经递质释放所必需的过程。这些发现有助于解释与 REMSD 相关的神经递质释放增加的细胞内机制。
