Charifi C, Paut-Pagano L, Debilly G, Cespuglio R, Jouvet M, Valatx J L
Département de Médecine Expérimentale, INSERM U480, Université Claude Bernard, 8 Avenue Rockefeller, 69373, cedex 08, Lyon, France.
Neurosci Lett. 2000 Jun 16;287(1):41-4. doi: 10.1016/s0304-3940(00)01106-x.
We previously showed that the noradrenergic locus coeruleus (NA-LC) was involved in the regulatory mechanisms of the paradoxical sleep rebound following a 10 h sleep deprivation by using a systemic injection of a specific neurotoxin, N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4). Given that rebound mechanisms are mainly located in the forebrain, we planned to study the role of the forebrain structures receiving LC afferences. In this study we evaluated the involvement of noradrenergic afferences to the central nucleus of the amygdala in the sleep rebound by DSP-4 microinjections into the central nucleus of the rat amygdala. The results showed that during the first recovery day, the paradoxical sleep rebound is lower in DSP-4 treated rats (-67.28%). These findings indicate that the amygdala, through its NA afferents, contributes to the sleep rebound mechanisms.
我们之前通过全身注射一种特定的神经毒素N-(2-氯乙基)-N-乙基-2-溴苄胺（DSP-4）表明，去甲肾上腺素能蓝斑核（NA-LC）参与了10小时睡眠剥夺后异相睡眠反弹的调节机制。鉴于反弹机制主要位于前脑，我们计划研究接受蓝斑核传入纤维的前脑结构的作用。在本研究中，我们通过向大鼠杏仁核中央核微量注射DSP-4，评估了杏仁核中央核去甲肾上腺素能传入纤维在睡眠反弹中的作用。结果显示，在第一个恢复日，经DSP-4处理的大鼠的异相睡眠反弹较低（-67.28%）。这些发现表明，杏仁核通过其去甲肾上腺素能传入纤维，对睡眠反弹机制有贡献。
