研究揭示海馬CA2區在社交記憶中的作用
作者:
小柯機器人發布時間:2020/10/22 13:36:21
美國哥倫比亞大學Steven A. Siegelbaum團隊取得最新進展。他們研究了海馬CA2區社交新穎性的編碼及其在22q11.2微缺失小鼠模型中的破壞和拯救。相關論文於2020年10月19日發表於《自然-神經科學》。
為了確定CA2活性是否編碼社交互動,他們在社交行為期間從雄性小鼠的CA2錐體神經元(PNs)進行細胞外記錄。儘管CA2神經元放電僅顯示出較弱的空間選擇性,但它可以準確地編碼環境變化,並可以區分新小鼠和熟悉的小鼠。在人類22q11.2微缺失的Df(16)A +/-小鼠模型中,精神分裂症的風險增加了30倍,CA2社交編碼受損,與這些小鼠中觀察到的社交記憶缺陷一致,但是空間編碼精度大大提高。
先前發現CA2 PNs在Df(16)A +/-小鼠中超極化,可能是由於TREK-1 K +電流的上調所致。他們發現TREK-1阻滯物拯救了Df(16)A +/-小鼠的社交記憶和CA2社交編碼,並支持CA2在社交刺激的正常編碼和疾病中社交行為障礙中的關鍵作用。
據悉,海馬CA2區對於社交記憶至關重要。
附:英文原文
Title: Coding of social novelty in the hippocampal CA2 region and its disruption and rescue in a 22q11.2 microdeletion mouse model
Author: Macayla L. Donegan, Fabio Stefanini, Torcato Meira, Joshua A. Gordon, Stefano Fusi, Steven A. Siegelbaum
Issue&Volume: 2020-10-19
Abstract: The hippocampal CA2 region is essential for social memory. To determine whether CA2 activity encodes social interactions, we recorded extracellularly from CA2 pyramidal neurons (PNs) in male mice during social behavior. Although CA2 neuronal firing showed only weak spatial selectivity, it accurately encoded contextual changes and distinguished between a novel and a familiar mouse. In the Df(16)A+/ mouse model of the human 22q11.2 microdeletion, which confers a 30-fold increased risk of schizophrenia, CA2 social coding was impaired, consistent with the social memory deficit observed in these mice; in contrast, spatial coding accuracy was greatly enhanced. CA2 PNs were previously found to be hyperpolarized in Df(16)A+/ mice, likely due to upregulation of TREK-1 K+ current. We found that TREK-1 blockade rescued social memory and CA2 social coding in Df(16)A+/ mice, supporting a crucial role for CA2 in the normal encoding of social stimuli and in social behavioral dysfunction in disease.
DOI: 10.1038/s41593-020-00720-5
Source: https://www.nature.com/articles/s41593-020-00720-5