Regulation of nociception by long-term potentiation of inhibitory postsynaptic currents from insular cortical parvalbumin-immunopositive neurons to pyramidal neurons.

IF 5.9 1区 医学 Q1 ANESTHESIOLOGY PAIN® Pub Date : 2025-01-21 DOI:10.1097/j.pain.0000000000003518
Satomi Kobayashi, Hironobu Osaki, Shigeki Kato, Kazuto Kobayashi, Masayuki Kobayashi
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Abstract

Abstract: The insular cortex (IC) processes various sensory information, including nociception, from the trigeminal region. Repetitive nociceptive inputs from the orofacial area induce plastic changes in the IC. Parvalbumin-immunopositive neurons (PVNs) project to excitatory neurons (pyramidal neurons [PNs]), whose inputs strongly suppress the activities of PNs. This study investigated how PVNs in the IC modulate pain-related behaviors using optogenetics. To evaluate the effect of PVN activation on pain-related behavior, we applied nociceptive heat stimulation to the whisker pads of PV-Cre rats that received an injection of adeno-associated virus-Flex-channelrhodopsin-2-mCherry into the IC. Exposure to nociceptive heat stimulation significantly increased the amount of pain-related escape behavior, and PVN activation by optogenetics did not significantly decrease pain-related behavior. We next examined the possibility that long-term potentiation (LTP) of PVN→PN synapses suppresses pain-related behaviors. We recorded light-evoked inhibitory postsynaptic currents (IPSCs) from PNs in the IC slice preparation to examine whether optogenetic activation of PVNs can induce LTP. Repetitive optogenetic stimulation (ROS) of PVNs in a manner analogous to theta burst stimulation increased the amplitude of IPSCs for at least 50 minutes. Long-term potentiation was induced by either the -45 or -60 mV membrane potential of PNs. Then, the IC received ROS to induce LTP of IPSCs from PVNs to PNs, and we evaluated pain-related behaviors. Compared to those before ROS, the pain-related behaviors were further reduced after ROS. These results suggest that LTP induction of PVN→PN synapses in the IC could be a possible treatment for abnormal pain in the orofacial area.

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从岛叶皮质小蛋白免疫阳性神经元到锥体神经元的抑制性突触后电流的长期增强对伤害感觉的调节。
摘要:岛叶皮层(IC)处理来自三叉神经区的各种感觉信息,包括伤害感受。来自口面部区域的重复性伤害性输入诱导IC的可塑性变化。细小蛋白免疫阳性神经元(PVNs)投射到兴奋性神经元(锥体神经元[PNs]),其输入强烈抑制PNs的活动。本研究利用光遗传学研究了IC内pvn如何调节疼痛相关行为。为了评估PVN激活对疼痛相关行为的影响,我们将痛觉性热刺激应用于PV-Cre大鼠的须片,这些大鼠注射了腺相关病毒-弯曲通道视紫红质-2- mcherry。暴露于痛觉性热刺激显著增加了疼痛相关逃避行为的数量,而光遗传学激活PVN并没有显著减少疼痛相关行为。接下来,我们研究了PVN→PN突触的长期增强(LTP)抑制疼痛相关行为的可能性。我们在IC片制备过程中记录了PNs的光诱发抑制性突触后电流(IPSCs),以检验光遗传激活PVNs是否可以诱导LTP。以类似于θ波爆发刺激的方式对PVNs进行重复光遗传刺激(ROS),可使IPSCs的振幅增加至少50分钟。PNs的-45 mV和-60 mV膜电位均可诱导长时程增强。然后,IC接受ROS诱导IPSCs从PVNs到PNs的LTP,并评估疼痛相关行为。与ROS前相比,ROS后疼痛相关行为进一步减少。这些结果表明,LTP诱导IC中PVN→PN突触可能是治疗口面部异常疼痛的一种可能方法。
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来源期刊
PAIN®
PAIN® 医学-临床神经学
CiteScore
12.50
自引率
8.10%
发文量
242
审稿时长
9 months
期刊介绍: PAIN® is the official publication of the International Association for the Study of Pain and publishes original research on the nature,mechanisms and treatment of pain.PAIN® provides a forum for the dissemination of research in the basic and clinical sciences of multidisciplinary interest.
期刊最新文献
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