Biochemical effects induced by REM sleep deprivation in naive and in D-amphetamine treated rats.

Neurobiology (Budapest, Hungary) Pub Date : 1998-01-01
A Lara-Lemus, R Drucker-Colín, J Méndez-Franco, M Palomero-Rivero, M Pérez de la Mora
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Abstract

The neurochemical dysfunction present in patients showing self-mutilating behavior (SMB) is not well understood. In animal models, rapid eye movement (REM) sleep deprivation enhances the SMB induced by the chronic administration of d-amphetamine. To understand the mechanism underlying these effects the levels of dopamine (DA), noradrenaline (NA) and serotonin (5-HT) were measured in REM sleep deprived only, and in REM sleep deprived and d-amphetamine treated rats. DA levels were elevated (31%) after REM sleep deprivation (48 h) in the neostriatum and the cerebral cortex (33%), while the levels of NA and 5-HT remained constant. A 6-day treatment with d-amphetamine (7.5 mg/kg; i.p.) failed to affect, in REM sleep deprived rats, DA, NA and 5-HT levels. It was also found that REM sleep deprivation had no effects on the d-amphetamine induced [3H]DA release from slices of the same regions. Our results suggests that dopaminergic mechanisms are involved in the effects of REM sleep deprivation on SMB.

d -安非他明处理大鼠和未处理大鼠REM睡眠剥夺后的生化效应。
自残行为(SMB)患者的神经化学功能障碍尚不清楚。在动物模型中,快速眼动(REM)睡眠剥夺可增强长期服用d-安非他明诱导的SMB。为了了解这些影响背后的机制,我们测量了仅在剥夺REM睡眠的大鼠以及剥夺REM睡眠和服用d-安非他明的大鼠的多巴胺(DA)、去甲肾上腺素(NA)和血清素(5-HT)的水平。REM睡眠剥夺(48 h)后,新纹状体和大脑皮层DA水平升高(31%),而NA和5-HT水平保持不变(33%)。d-安非他明治疗6天(7.5 mg/kg;在快速眼动睡眠剥夺的大鼠中,DA、NA和5-羟色胺水平没有受到影响。研究还发现,REM睡眠剥夺对d-安非他明诱导的[3H]DA从同一区域的切片释放没有影响。我们的研究结果表明,多巴胺能机制参与了快速眼动睡眠剥夺对SMB的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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