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幼年应激对成年大鼠海马 CA2 可塑性和社交记忆的影响。

Alteration of hippocampal CA2 plasticity and social memory in adult rats impacted by juvenile stress.

机构信息

Department of Physiology, National University of Singapore, Singapore, 117593, Singapore.

Life Sciences Institute Neurobiology Programme, Centre for Life Sciences, National University of Singapore, Singapore, 117456, Singapore.

出版信息

Hippocampus. 2023 Jun;33(6):745-758. doi: 10.1002/hipo.23531. Epub 2023 Mar 25.

DOI:10.1002/hipo.23531
PMID:36965045
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10946601/
Abstract

The hippocampal CA2 region has received greater attention in recent years due to its fundamental role in social memory and hippocampus-dependent memory processing. Unlike entorhinal cortical inputs, the Schaffer collateral inputs to CA2 do not support activity-dependent long-term potentiation (LTP), which serves as the basis for long-term memories. This LTP-resistant zone also expresses genes that restrict plasticity. With the aim of exploring social interaction and sociability in rats that were subjected to juvenile stress, we addressed questions about how the neural circuitry is altered and its effects on social behavior. Although there was induction of LTP in both Schaffer collateral and entorhinal cortical pathways in juvenile-stressed rats, LTP declined in both pathways after 2-3 h. Moreover, exogenous bath application of substance P, a neuropeptide that resulted in slow onset long-lasting potentiation in control animals while it failed to induce LTP in juvenile-stressed rats. Our study reveals that juvenile-stressed rats show behavioral and cellular abnormalities with a long-lasting impact in adulthood.

摘要

近年来,由于 CA2 区在社会记忆和海马依赖的记忆处理中起着基础性作用,因此受到了更多的关注。与内嗅皮层的传入不同,CA2 区的 Schaffer 侧枝传入不支持活动依赖性长时程增强(LTP),而后者是长时记忆的基础。这个 LTP 抗性区也表达了限制可塑性的基因。为了探索经历过青少年期应激的大鼠的社会互动和社交能力,我们提出了一些问题,即神经回路如何发生改变,以及其对社会行为的影响。尽管在青少年应激大鼠的 Schaffer 侧枝和内嗅皮层通路上都诱导了 LTP,但在 2-3 小时后,两条通路上的 LTP 都下降了。此外,外源性应用神经肽物质 P 也未能诱导 LTP,而物质 P 会导致对照动物中出现缓慢起始的长时程增强。我们的研究表明,青少年期应激大鼠在成年后表现出行为和细胞异常,并具有持久的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b0c/10946601/b182564fdaef/HIPO-33-745-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b0c/10946601/7f8d05dff776/HIPO-33-745-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b0c/10946601/f116cd12f556/HIPO-33-745-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b0c/10946601/68c08d095f73/HIPO-33-745-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b0c/10946601/b182564fdaef/HIPO-33-745-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b0c/10946601/7f8d05dff776/HIPO-33-745-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b0c/10946601/f116cd12f556/HIPO-33-745-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b0c/10946601/68c08d095f73/HIPO-33-745-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b0c/10946601/b182564fdaef/HIPO-33-745-g004.jpg

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