激活精氨酸加压素受体1a可降低小鼠附属嗅球互惠突触的抑制性突触电流

IF 4.2 3区 医学 Q2 NEUROSCIENCES
Frontiers in Cellular Neuroscience Pub Date : 2024-09-24 eCollection Date: 2024-01-01 DOI:10.3389/fncel.2024.1466817
Mutsuo Taniguchi, Yoshihiro Murata, Masahiro Yamaguchi, Hideto Kaba
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引用次数: 0

摘要

中枢精氨酸加压素(AVP)可促进哺乳动物的社会识别并调节其许多复杂的社会行为,在许多情况下,这些行为是根据嗅觉和/或信息素信号相互识别的。AVP神经元存在于附属嗅球(AOB)中,AOB是绒球嗅觉系统的第一个中继站,已被证实是雌性小鼠交配诱导的配偶识别(嗅觉记忆)的关键场所。从 AOB 到高级中枢的信息传递受树枝状递质递归抑制的控制,即抑制性突触后电流(IPSCs)由颗粒细胞的递归树枝状抑制性输入在丝裂细胞中产生。这些报道表明,AVP 可能在调节 AOB 的树突抑制中发挥重要作用。为了验证这一假设,我们研究了在23-36天大的Balb/c小鼠的切片制备中,细胞外施用AVP对从有丝分裂和颗粒细胞测得的突触反应的影响。为了唤起有丝分裂细胞的树突抑制,我们采用传统的全细胞配置,向有丝分裂细胞施加-70至0 mV的去极化电压(持续时间为10 ms)。我们发现,AVP 能明显降低 IPSCs。血管加压素受体 1a(V1aR)拮抗剂(Manning 复合物)可减轻 AVP 对 IPSCs 的抑制作用,但血管加压素受体 1b 拮抗剂(SSR149415)则不会。V1aRs的激动剂[(Phe2)OVT]模拟了AVP对IPSCs的作用。此外,AVP 还能明显抑制颗粒细胞中的电压激活电流,而不影响有丝分裂细胞对γ-氨基丁酸(GABA)的反应幅度。本研究结果表明,V1aRs 通过突触前机制减少颗粒细胞的 GABA 能传导,从而在小鼠 AOB 有丝分裂细胞和颗粒细胞之间的相互传导中发挥作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Activation of arginine vasopressin receptor 1a reduces inhibitory synaptic currents at reciprocal synapses in the mouse accessory olfactory bulb.

Central arginine vasopressin (AVP) facilitates social recognition and modulates many complex social behaviors in mammals that, in many cases, recognize each other based on olfactory and/or pheromonal signals. AVP neurons are present in the accessory olfactory bulb (AOB), which is the first relay in the vomeronasal system and has been demonstrated to be a critical site for mating-induced mate recognition (olfactory memory) in female mice. The transmission of information from the AOB to higher centers is controlled by the dendrodendritic recurrent inhibition, i.e., inhibitory postsynaptic currents (IPSCs) generated in mitral cells by recurrent dendrodendritic inhibitory inputs from granule cells. These reports suggest that AVP might play an important role in regulating dendrodendritic inhibition in the AOB. To test this hypothesis, we examined the effects of extracellularly applied AVP on synaptic responses measured from mitral and granule cells in slice preparations from 23--36-day-old Balb/c mice. To evoke dendrodendritic inhibition in a mitral cell, depolarizing voltages of -70 to 0 mV (10 ms duration) were applied to a mitral cell using a conventional whole-cell configuration. We found that AVP significantly reduced the IPSCs. The suppressive effects of AVP on the IPSCs was diminished by an antagonist for vasopressin receptor 1a (V1aR) (Manning compound), but not by an antagonist for vasopressin receptor 1b (SSR149415). An agonist for V1aRs [(Phe2)OVT] mimicked the action of AVP on IPSCs. Additionally, AVP significantly suppressed voltage-activated currents in granule cells without affecting the magnitude of the response of mitral cells to gamma-aminobutyric acid (GABA). The present results suggest that V1aRs play a role in reciprocal transmission between mitral cells and granule cells in the mouse AOB by reducing GABAergic transmission through a presynaptic mechanism in granule cells.

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来源期刊
CiteScore
7.90
自引率
3.80%
发文量
627
审稿时长
6-12 weeks
期刊介绍: Frontiers in Cellular Neuroscience is a leading journal in its field, publishing rigorously peer-reviewed research that advances our understanding of the cellular mechanisms underlying cell function in the nervous system across all species. Specialty Chief Editors Egidio D‘Angelo at the University of Pavia and Christian Hansel at the University of Chicago are supported by an outstanding Editorial Board of international researchers. This multidisciplinary open-access journal is at the forefront of disseminating and communicating scientific knowledge and impactful discoveries to researchers, academics, clinicians and the public worldwide.
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