Coordination between midcingulate cortex and retrosplenial cortex in pain regulation

IF 3.5 3区 医学 Q2 NEUROSCIENCES Frontiers in Molecular Neuroscience Pub Date : 2024-08-06 DOI:10.3389/fnmol.2024.1405532
Yunya Qiu, Yan-Na Lian, Cheng Wu, Li Liu, Chen Zhang, Xiang-Yao Li
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Abstract

IntroductionThe cingulate cortex, with its subregions ACC, MCC, and RSC, is key in pain processing. However, the detailed interactions among these regions in modulating pain sensation have remained unclear.MethodsIn this study, chemogenetic tools were employed to selectively activate or inhibit neuronal activity in the MCC and RSC of rodents to elucidate their roles in pain regulation.Results: Our results showed that chemogenetic activation in both the RSC and MCC heightened pain sensitivity. Suppression of MCC activity disrupted the RSC’s regulation of both mechanical and thermal pain, while RSC inhibition specifically affected the MCC’s regulation of thermal pain.DiscussionThe findings indicate a complex interplay between the MCC and RSC, with the MCC potentially governing the RSC’s pain regulatory mechanisms. The RSC, in turn, is crucial for the MCC’s control over thermal sensation, revealing a collaborative mechanism in pain processing.ConclusionThis study provides evidence for the MCC and RSC’s collaborative roles in pain regulation, highlighting the importance of their interactions for thermal and mechanical pain sensitivity. Understanding these mechanisms could aid in developing targeted therapies for pain disorders.
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中脑皮层和后脾皮层在疼痛调节中的协调作用
引言 带状皮层及其亚区域 ACC、MCC 和 RSC 是疼痛处理的关键。本研究利用化学遗传学工具选择性地激活或抑制啮齿类动物扣带回皮层(MCC)和扣带回皮层(RSC)的神经元活动,以阐明它们在疼痛调节中的作用:结果:我们的研究结果表明,化学基因激活 RSC 和 MCC 可提高疼痛敏感性。讨论:研究结果表明,MCC 和 RSC 之间存在复杂的相互作用,MCC 有可能控制 RSC 的疼痛调节机制。反过来,RSC 对 MCC 对热感觉的控制也至关重要,这揭示了疼痛处理过程中的一种协作机制。了解这些机制有助于开发治疗疼痛疾病的靶向疗法。
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来源期刊
CiteScore
5.70
自引率
2.10%
发文量
669
审稿时长
14 weeks
期刊介绍: Frontiers in Molecular Neuroscience is a first-tier electronic journal devoted to identifying key molecules, as well as their functions and interactions, that underlie the structure, design and function of the brain across all levels. The scope of our journal encompasses synaptic and cellular proteins, coding and non-coding RNA, and molecular mechanisms regulating cellular and dendritic RNA translation. In recent years, a plethora of new cellular and synaptic players have been identified from reduced systems, such as neuronal cultures, but the relevance of these molecules in terms of cellular and synaptic function and plasticity in the living brain and its circuits has not been validated. The effects of spine growth and density observed using gene products identified from in vitro work are frequently not reproduced in vivo. Our journal is particularly interested in studies on genetically engineered model organisms (C. elegans, Drosophila, mouse), in which alterations in key molecules underlying cellular and synaptic function and plasticity produce defined anatomical, physiological and behavioral changes. In the mouse, genetic alterations limited to particular neural circuits (olfactory bulb, motor cortex, cortical layers, hippocampal subfields, cerebellum), preferably regulated in time and on demand, are of special interest, as they sidestep potential compensatory developmental effects.
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