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前扣带回皮层中通过降低 Ih 增强树突整合会增加痛觉感受。

Enhanced dendritic integration by ih reduction in the anterior cingulate cortex increases nociception.

作者信息

Dickinson Jasmine R, Scherrer Grégory

机构信息

Department of Anesthesiology, Perioperative and Pain Medicine, Department of Molecular and Cellular Physiology, Department of Neurosurgery, Stanford Neurosciences Institute, Stanford University, Palo Alto, CA 94304, USA; Biology Graduate Program, Stanford University, Stanford, CA 94305, USA.

Department of Anesthesiology, Perioperative and Pain Medicine, Department of Molecular and Cellular Physiology, Department of Neurosurgery, Stanford Neurosciences Institute, Stanford University, Palo Alto, CA 94304, USA.

出版信息

Neuron. 2015 Apr 8;86(1):4-6. doi: 10.1016/j.neuron.2015.03.045.

DOI:10.1016/j.neuron.2015.03.045
PMID:25856476
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7341066/
Abstract

In this issue of Neuron, Santello and Nevian (2015) report HCN channel plasticity and increased temporal summation in layer 5 ACC neurons following nerve injury. They are able to restore HCN channel function and reduce behavioral hypersensitivity with selective serotonin receptor targeting.

摘要

在本期《神经元》杂志中,桑泰洛和内维安(2015年)报告了神经损伤后5层前扣带回皮质(ACC)神经元中HCN通道可塑性及时间总和增加的情况。他们通过靶向选择性5-羟色胺受体,能够恢复HCN通道功能并减轻行为超敏反应。

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Enhanced dendritic integration by ih reduction in the anterior cingulate cortex increases nociception.前扣带回皮层中通过降低 Ih 增强树突整合会增加痛觉感受。
Neuron. 2015 Apr 8;86(1):4-6. doi: 10.1016/j.neuron.2015.03.045.
2
Dysfunction of cortical dendritic integration in neuropathic pain reversed by serotoninergic neuromodulation.皮层树突整合功能障碍在神经病理性疼痛中被 5-羟色胺能神经调质调节逆转。
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Activation of mGluR1 contributes to neuronal hyperexcitability in the rat anterior cingulate cortex via inhibition of HCN channels.代谢型谷氨酸受体1(mGluR1)的激活通过抑制超极化激活的环核苷酸门控(HCN)通道,导致大鼠前扣带皮层神经元兴奋性过高。
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[Changes in the cortical neuronal dendrites in experimental alcoholic intoxication].
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本文引用的文献

1
Dysfunction of cortical dendritic integration in neuropathic pain reversed by serotoninergic neuromodulation.皮层树突整合功能障碍在神经病理性疼痛中被 5-羟色胺能神经调质调节逆转。
Neuron. 2015 Apr 8;86(1):233-46. doi: 10.1016/j.neuron.2015.03.003. Epub 2015 Mar 26.
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Coexistence of two forms of LTP in ACC provides a synaptic mechanism for the interactions between anxiety and chronic pain.ACC 中两种形式的 LTP 的共存为焦虑和慢性疼痛之间的相互作用提供了一种突触机制。
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HCN2 ion channels play a central role in inflammatory and neuropathic pain.
HCN2 离子通道在炎症性和神经性疼痛中起核心作用。
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Presynaptic and postsynaptic amplifications of neuropathic pain in the anterior cingulate cortex.前扣带回皮层中神经性疼痛的突触前和突触后放大
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Upregulation of forebrain NMDA NR2B receptors contributes to behavioral sensitization after inflammation.前脑NMDA NR2B受体的上调促成炎症后的行为敏化。
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Prolonged membrane potential depolarization in cingulate pyramidal cells after digit amputation in adult rats.成年大鼠断指后扣带回锥体细胞的膜电位长期去极化
Mol Pain. 2005 Aug 19;1:23. doi: 10.1186/1744-8069-1-23.
9
A behavioral role for dendritic integration: HCN1 channels constrain spatial memory and plasticity at inputs to distal dendrites of CA1 pyramidal neurons.树突整合的行为作用:HCN1通道限制CA1锥体神经元远端树突输入处的空间记忆和可塑性。
Cell. 2004 Nov 24;119(5):719-32. doi: 10.1016/j.cell.2004.11.020.
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Glutamatergic activation of anterior cingulate cortex produces an aversive teaching signal.前扣带回皮质的谷氨酸能激活产生厌恶教学信号。
Nat Neurosci. 2004 Apr;7(4):398-403. doi: 10.1038/nn1207. Epub 2004 Mar 7.