Neurophysiological analysis of sleep regulation mechanism through the basal ganglion-pontine tegmental systems

基底神经节-桥脑被盖系统睡眠调节机制的神经生理学分析

• 批准号: 17605003
• 负责人: KOYAMA Yoshimasa
• 金额: $ 2.3万
• 依托单位: Fukushima University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2005
• 资助国家: 日本
• 起止时间: 2005 至 2006
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-17605003/
• 关键词: substantia nigra pars reticulata; acetylcholine neuron; pedunculopontine tegmental nucleus; orexin; basal ganglia; lateral hypothalamus; muscular tonus; GABA; アセチルコリンニューロン; 脚橋被蓋核; 外背側被蓋核

The pontine tegmental area has a crucial role in regulation of REM sleep and wakefulness. The basal ganglia is, projecting to the pontine tegmental area, involved in motor regulation or regulation of muscular tonus. The orexinergic system in the hypothalamus project to the basal ganglia (substantia nigra pars reticulata : SNr) or the pontine tegmentum and regulate the various events during sleep and wakefulness. The present study was performed to elucidate the sleep regulation mechanisms especially the relation of muscular tonus regulation mediated by the hypothalamic-basal ganglia axis. The results obtained are ;1.In decebrated cats, activation of the SNr by orexin injection increased or maintained the muscular tonus level ; muscular atonia induced by the electrical stimulation to the pedunculopontine tegmental nucleus (PPN) was suppressed after the orexin injection to the SNr. The orexin effect was blocked by bicuculline (GABA_A receptor antagonist). The same effect was obtained when orexin was injected to the PPN. These results suggest that the GABAergic neurons in the SNr or the GABAergic interneurons in the PPN regulate the muscular tonus by suppressing the PPN neurons that initiate muscular atonia.2.When orexin was injected to the PPN in free moving rats, GABA release measured by microdialysis method increased. The result supports the hypothesis that the there is a tonic GABAergic inhibition on the PPN neurons that is mediated by the orexinergic influence to the SNr or PPN.3.The GABAergic neurons in the SNr showed higher activity during wakefulness or bpoth wakefulness and REM sleep. These neurons are candidates of the GABAergic input to the PPN that suppress the atonia inducing system in the PPN during wakefulness.

脑桥被盖区在REM睡眠和觉醒的调节中起着至关重要的作用。基底神经节投射到脑桥被盖区，参与运动调节或肌肉紧张的调节。下丘脑中的食欲素能系统投射到基底神经节（黑质网状部：SNr）或脑桥被盖，并调节睡眠和觉醒期间的各种事件。本研究旨在阐明下丘脑-基底节轴介导的睡眠调节机制，特别是与肌张力调节的关系。得到的结果是：1.在去神经猫，注射食欲素激活SNr可增加或维持肌张力水平，电刺激脚桥被盖核（PPN）引起的肌张力减弱在SNr注射食欲素后被抑制。GABA_A受体拮抗剂荷包牡丹碱（bicuculline）可阻断增食欲素的作用。当将食欲素注射到PPN时，获得了相同的效果。提示SNr内GABA能神经元或PPN内GABA能中间神经元通过抑制启动肌张力的PPN神经元来调节肌张力。2.在自由活动大鼠的PPN内注射orexin后，微透析法测定GABA释放量增加。实验结果支持了PPN神经元的紧张性GABA能抑制的假说，这种抑制是由食欲素能影响SNr或PPN神经元介导的。这些神经元是GABA能输入到PPN的候选者，其在觉醒期间抑制PPN中的张力缺乏诱导系统。

项目成果

Requirement of tryptophan hydroxylase during development for maturation of sensorimotor gating

• DOI: 10.1016/j.jmb.2006.08.051
• 发表时间: 2006-10-20
• 期刊: JOURNAL OF MOLECULAR BIOLOGY
• 影响因子: 5.6
• 作者: Nakamura, Kazuhiro;Koyama, Yoshimasa;Hirose, Sachiko
• 通讯作者: Hirose, Sachiko

A quartet neural system model orchestrating sleep and wakefulness mechanisms.

• DOI: 10.1152/jn.00575.2005
• 发表时间: 2006-04
• 期刊: Journal of neurophysiology
• 影响因子: 2.5
• 作者: Yuichi Tamakawa;A. Karashima;Y. Koyama;N. Katayama;M. Nakao

Input of orexin/hypocretin neurons revealed by genetically encoded tracer in mice.

基因编码示踪剂揭示小鼠食欲素/下丘脑分泌素神经元的输入。

• 发表时间: 2005
• 期刊: Neuron 46
• 作者: Sakurai T;Nagata R;Yamanaka A;Kawamura H;Tsujino N;Muraki Y;Kageyama H;Kunita S;Takahashi S;Goto K;Koyama T;Shioda S;Yanagisawa M.
• 通讯作者: Yanagisawa M.

The orexinergic synaptic innervation of serotonin- and orexin 1receptor-containig neurons in the dorsal raphe nucleus.

中缝背核中含有血清素和食欲素 1 受体的神经元的食欲素能突触神经支配。

• 发表时间: 2005
• 期刊: Reg. Peptide 126
• 作者: Wang Q.-P.;Koyama Y.;Guan J.-L.;Kayama Y.;Takahashi K.;Kayama Y.;Shioda S.
• 通讯作者: Shioda S.

Neurobiological basis of state-dependent control of motor behaviors

运动行为状态依赖性控制的神经生物学基础

• 发表时间: 2006
• 期刊: Sleep Biol Rhythms 4
• 作者: Takakusaki K.;Saito K.;Nonaka T.;Okumura T.;Miyokawa N.;Koyama Y.
• 通讯作者: Koyama Y.