Differential expression of long-term depression, and synaptic tagging and capture in mouse hippocampal area CA2 synapses.

IF 3.8 Q2 MULTIDISCIPLINARY SCIENCES
PNAS nexus Pub Date : 2025-07-29 eCollection Date: 2025-08-01 DOI:10.1093/pnasnexus/pgaf241
Zijun Wang, Lik-Wei Wong, Sreedharan Sajikumar
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Abstract

CA2 hippocampal neurons have received renewed interest due to their unique functions and plasticity properties that differ between synapses within the same neuronal population. However, detailed studies on long-term depression (LTD) in CA2 pyramidal neurons are lacking. In this study, LTD was induced and characterized at both Schaffer collateral-CA2 (SC-CA2) and entorhinal cortex-CA2 (EC-CA2) synapses in young, male mice. This LTD was found to be dependent on N-methyl-D-aspartate receptors, protein synthesis, and p75 neurotrophin receptors. However, weaker stimulations could only induce early LTD in EC-CA2 but not SC-CA2 synapses, consistent with its "plasticity-resistant" nature. CA2 LTD is capable of undergoing heterosynaptic synaptic tagging and capture (STC), although the machinery involved differs between SC-CA2 and EC-CA2 synapses. SC-CA2, but not EC-CA2, requires precursor brain-derived neurotrophic factor activity to maintain LTD. Subsequently, quantitative shotgun proteomics analysis yields complexin-2 as a strong candidate plasticity-related product involved in LTD in the CA2. These results reveal interesting differences in STC machinery between synaptic populations of a common set of neurons, enhancing our understanding of hippocampal circuitry involving the CA2. Interesting implications regarding the heterogeneous biochemical makeup of CA2 pyramidal neurons and fundamental STC theory that arise as a consequent of our results are also discussed further.

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小鼠海马区CA2突触的长期抑郁、突触标记和捕获的差异表达。
CA2海马神经元因其独特的功能和可塑性特性而重新受到关注,这些特性在同一神经元群体中的突触之间存在差异。然而,关于CA2锥体神经元长期抑制(LTD)的详细研究尚缺乏。在这项研究中,LTD在年轻雄性小鼠的Schaffer侧侧ca2 (SC-CA2)和内嗅皮质ca2 (EC-CA2)突触中被诱导和表征。这种LTD被发现依赖于n -甲基- d -天冬氨酸受体、蛋白质合成和p75神经营养因子受体。然而,较弱的刺激只能诱导EC-CA2突触的早期LTD,而不能诱导SC-CA2突触的早期LTD,这与其“抗可塑性”的性质一致。CA2 LTD能够经历异突触突触标记和捕获(STC),尽管SC-CA2和EC-CA2突触之间涉及的机制不同。SC-CA2,而不是EC-CA2,需要前体脑源性神经营养因子活性来维持LTD。随后,定量霰弹枪蛋白质组学分析得出复杂蛋白-2是参与CA2中LTD的强候选可塑性相关产物。这些结果揭示了一组常见神经元突触群之间STC机制的有趣差异,增强了我们对涉及CA2的海马回路的理解。关于CA2锥体神经元的异质生化组成和基本STC理论的有趣含义,作为我们的结果的结果也进一步讨论。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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CiteScore
1.80
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