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脊髓中抑制作用的可塑性。

Plasticity of inhibition in the spinal cord.

作者信息

Todd Andrew J

机构信息

Institute of Neuroscience and Psychology, College of Medical Veterinary and Life Sciences, University of Glasgow, Glasgow, G12 8QQ, UK,

出版信息

Handb Exp Pharmacol. 2015;227:171-90. doi: 10.1007/978-3-662-46450-2_9.

Abstract

Inhibitory interneurons, which use GABA and/or glycine as their principal transmitter, have numerous roles in regulating the transmission of sensory information through the spinal dorsal horn. These roles are likely to be performed by different populations of interneurons, each with specific locations in the synaptic circuitry of the region. Peripheral nerve injury frequently leads to neuropathic pain, and it is thought that loss of function of inhibitory interneurons in the dorsal horn contributes to this condition. Several mechanisms have been proposed for this disinhibition, including death of inhibitory interneurons, decreased transmitter release, diminished activity of these cells and reduced effectiveness of GABA and glycine as inhibitory transmitters. However, despite numerous studies on this important topic, it is still not clear which (if any) of these mechanisms contributes to neuropathic pain after nerve injury.

摘要

抑制性中间神经元以γ-氨基丁酸(GABA)和/或甘氨酸作为主要神经递质,在调节感觉信息通过脊髓背角的传递过程中发挥着多种作用。这些作用可能由不同群体的中间神经元来执行,每个群体在该区域的突触回路中都有特定的位置。周围神经损伤常导致神经性疼痛,人们认为背角中抑制性中间神经元的功能丧失促成了这种情况。针对这种去抑制现象已经提出了几种机制,包括抑制性中间神经元的死亡、神经递质释放减少、这些细胞的活性降低以及GABA和甘氨酸作为抑制性神经递质的效力降低。然而,尽管对这个重要课题进行了大量研究,但仍不清楚这些机制中哪一种(如果有的话)导致了神经损伤后的神经性疼痛。

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