Dopaminergic and cholinergic regulation of respiratory rhythm and anesthetic respiratory suppression mechanism

多巴胺能和胆碱能调节呼吸节律及麻醉呼吸抑制机制

基本信息

批准号：
13671595
负责人：
HAMAKAWA Toshiro
金额：
$ 2.3万
依托单位：
Miyazaki Medical College
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2001
资助国家：
日本
起止时间：
2001 至 2002
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-13671595/
关键词：
Dopamine Inhibitory synapse Excitatory synapse Lymnaea Volatile anesthetic Sevoflurane D2 receptor Lymmaea アセチルコリン

项目摘要

In this study, the identified dopaminergic excitatory synapse was reconstructed between the somata of two identified Lymnaea neurons, right pedal dorsal 1 (RPeD1 -the giant dopaminergic neuron ; presynaptic cell) and visceral dorsal, 2/3 (VD2/3 ; postsynaptic cell). Current clamp technique was used to determine whether clinically relevant concentrations (0.5-2%) of sevoflurane could block both the (synaptic) response of VD2/3 to depolarizing currents induced to RPeD land the (non-synaptic) responses of RPeD1 and VD2/3 to exogenously applied dopamine (DA). The application of DA (10 μ M) was directed to the soma-soma superfusing or non-superfusing sites on the synapse. Sevoflurane was found to suppress both synaptic and non synaptic DA responses in VD2/3 (0.5% ;>60%, 2% ;>90%), while weakly suppress the non synaptic DA response response in RPeD1. Sevoflurane's ability to suppress those responses was then comapred with DA antagonists. The D2 antagonist (+-) sulpiride almost completely (>85%) blocked those all responses in RPeD1 and VD2/3, though the general DA antagonist d-tubocurarine did not block only the non synaptic DA response in RPeD1. The effects of all drugs used did not differ the superfusing versus the non-superfusing sites of DA application. Our data demonstrate that sevoflurane-induced suppression of responses on the excitatory synapse between RPeD1 and VD2/3 is predominantly postsynaptic.

在本研究中，在两个已确定的 Lymnaea 神经元的体体之间重建了已确定的多巴胺能兴奋性突触，即右足背侧 1（RPeD1 - 巨型多巴胺能神经元；突触前细胞）和内脏背侧 2/3（VD2/3；突触后细胞） .电流钳技术用于确定七氟烷的临床相关浓度（0.5-2%）可以阻断 VD2/3 对 RPeD 诱导的去极化电流的（突触）反应，并阻断 RPeD1 和 VD2/3 对外源施加的多巴胺 (DA) 的（非突触）反应。 DA (10 μ M) 的应用是。发现针对突触上的体体-体体重叠或非重叠位点的七氟醚可以抑制突触和非突触。 VD2/3 中的 DA 反应（0.5%；>60%，2%；>90%），而 RPeD1 中的非突触 DA 反应则微弱地抑制，然后将七氟烷抑制这些反应的能力与 DA 拮抗剂进行比较。 (+-) 舒必利几乎完全 (>85%) 阻断了 RPeD1 和 VD2/3 中的所有反应，尽管一般 DA 拮抗剂d-筒箭毒碱不仅仅阻断 RPeD1 中的非突触 DA 反应。我们的数据表明，七氟烷诱导的兴奋性突触反应抑制在重叠位点与非重叠位点上没有差异。 RPeD1 和 VD2/3 之间的作用主要是突触后作用。