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反向神经血管耦联有助于全身稳态挑战期间血管加压素神经元的正反馈兴奋。

Inverse neurovascular coupling contributes to positive feedback excitation of vasopressin neurons during a systemic homeostatic challenge.

机构信息

Neuroscience Institute, Georgia State University, Atlanta, GA, USA.

Department of Physiology, University of Otago, Dunedin, New Zealand.

出版信息

Cell Rep. 2021 Nov 2;37(5):109925. doi: 10.1016/j.celrep.2021.109925.

DOI:10.1016/j.celrep.2021.109925
PMID:34731601
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9488983/
Abstract

Neurovascular coupling (NVC), the process that links neuronal activity to cerebral blood flow changes, has been mainly studied in superficial brain areas, namely the neocortex. Whether the conventional, rapid, and spatially restricted NVC response can be generalized to deeper and functionally diverse brain regions remains unknown. Implementing an approach for in vivo two-photon imaging from the ventral surface of the brain, we show that a systemic homeostatic challenge, acute salt loading, progressively increases hypothalamic vasopressin (VP) neuronal firing and evokes a vasoconstriction that reduces local blood flow. Vasoconstrictions are blocked by topical application of a VP receptor antagonist or tetrodotoxin, supporting mediation by activity-dependent, dendritically released VP. Salt-induced inverse NVC results in a local hypoxic microenvironment, which evokes positive feedback excitation of VP neurons. Our results reveal a physiological mechanism by which inverse NVC responses regulate systemic homeostasis, further supporting the notion of brain heterogeneity in NVC responses.

摘要

神经血管耦合 (NVC) 是将神经元活动与脑血流变化联系起来的过程,主要在大脑表面区域(即新皮层)进行研究。常规的、快速的、空间限制的 NVC 反应是否可以推广到更深层次和功能多样化的脑区仍然未知。我们采用一种从大脑腹表面进行体内双光子成像的方法,结果表明全身性的稳态挑战(急性盐负荷)会逐渐增加下丘脑血管加压素 (VP) 神经元的放电,并引起血管收缩,从而减少局部血流。VP 受体拮抗剂或河豚毒素的局部应用可阻断血管收缩,表明其由活动依赖性、树突释放的 VP 介导。盐诱导的反向 NVC 导致局部缺氧微环境,从而引发 VP 神经元的正反馈兴奋。我们的结果揭示了反向 NVC 反应调节全身稳态的生理机制,进一步支持了 NVC 反应中脑异质性的观点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d496/9488983/b277adc385aa/nihms-1753638-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d496/9488983/ff6d0ae6cd8a/nihms-1753638-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d496/9488983/2720115db825/nihms-1753638-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d496/9488983/e56db5980031/nihms-1753638-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d496/9488983/b277adc385aa/nihms-1753638-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d496/9488983/ff6d0ae6cd8a/nihms-1753638-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d496/9488983/2720115db825/nihms-1753638-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d496/9488983/e56db5980031/nihms-1753638-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d496/9488983/b277adc385aa/nihms-1753638-f0005.jpg

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