神经性疼痛会改变大鼠I层脊髓-臂旁神经元的输出。
Neuropathic pain changes the output of rat lamina I spino-parabrachial neurons.
作者信息
Krotov Volodymyr, Agashkov Kirill, Romanenko Sergii, Koroid Kostiantyn, Krasniakova Marharyta, Belan Pavel, Voitenko Nana
机构信息
Department of Sensory Signaling, Bogomoletz Institute of Physiology, NASU, Kyiv, Ukraine.
Department of Molecular Biophysics, Bogomoletz Institute of Physiology, NASU, Kyiv, Ukraine.
出版信息
BBA Adv. 2023 Feb 14;3:100081. doi: 10.1016/j.bbadva.2023.100081. eCollection 2023.
• Spared nerve injury (SNI) altered the action potential (AP) output of lamina I spino-parabrachial neurons (SPNs) without affecting their resting potential or membrane resistance. • In one-third of SPNs, high-threshold dorsal root stimulation elicited persistent AP firing which was never observed in cells from naïve animals. • 38% of SPNs from SNI rats showed spontaneous persistent AP firing. • After SNI low- and high-output SPNs were no longer nociceptive-specific as part of them responded with APs to low-threshold stimulation. • These SNI-induced changes of SPN output might represent cellular mechanisms for neuropathy-associated allodynia, hyperalgesia, and spontaneous pain.
• 保留神经损伤（SNI）改变了I层脊髓-臂旁神经元（SPN）的动作电位（AP）输出，而不影响其静息电位或膜电阻。
• 在三分之一的SPN中，高阈值背根刺激引发了持续性AP发放，这在未受伤动物的细胞中从未观察到。
• SNI大鼠中38%的SPN表现出自发性持续性AP发放。
• SNI后，低输出和高输出SPN不再具有伤害性特异性，因为其中一部分对低阈值刺激有AP反应。
• 这些由SNI引起的SPN输出变化可能代表了神经病变相关的感觉异常、痛觉过敏和自发痛的细胞机制。
Zotero 插件