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脑啡肽使大鼠海马体中的中间神经元超极化。

Enkephalin hyperpolarizes interneurones in the rat hippocampus.

作者信息

Madison D V, Nicoll R A

机构信息

Department of Pharmacology, University of California, San Francisco 94143.

出版信息

J Physiol. 1988 Apr;398:123-30. doi: 10.1113/jphysiol.1988.sp017033.

DOI:10.1113/jphysiol.1988.sp017033
PMID:3392667
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1191763/
Abstract
  1. Intracellular recordings were made from pyramidal cells and from electrophysiologically identified interneurones in the CA1 region of the hippocampal slice preparation from the rat. 2. Enkephalin blocked the hyperpolarization of pyramidal cells evoked by application of glutamate to synaptically coupled inhibitory interneurones. 3. Enkephalin hyperpolarized interneurones, most probably by increasing potassium conductance; this action was blocked by the opiate antagonist, naloxone. 4. Activation of gamma-aminobutyric acid(B) receptors with baclofen in interneurones produced a similar hyperpolarization that was resistant to naloxone. 5. In addition to hyperpolarizing interneurones, enkephalin blocked the inhibitory postsynaptic potential recorded in these cells. 6. These results suggest that opiate receptors are selectively localized on inhibitory interneurones in the hippocampus and are coupled to potassium channels. Activation of these receptors causes a disinhibition of both pyramidal cells and inhibitory interneurones.
摘要
  1. 在大鼠海马脑片制备物的CA1区域,从锥体细胞和经电生理鉴定的中间神经元进行细胞内记录。2. 脑啡肽阻断了通过向突触耦合的抑制性中间神经元施加谷氨酸所诱发的锥体细胞超极化。3. 脑啡肽使中间神经元超极化,最可能是通过增加钾电导;这种作用被阿片拮抗剂纳洛酮阻断。4. 在中间神经元中用巴氯芬激活γ-氨基丁酸(B)受体产生了类似的对纳洛酮有抗性的超极化。5. 除了使中间神经元超极化外,脑啡肽还阻断了在这些细胞中记录到的抑制性突触后电位。6. 这些结果表明阿片受体选择性地定位于海马中的抑制性中间神经元上,并与钾通道偶联。这些受体的激活导致锥体细胞和抑制性中间神经元的去抑制。

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本文引用的文献

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