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A Temporal Activity of CA1 Neurons Underlying Short-Term Memo
AAV-CaMKII-cre was used to generate PTEN CKO mouse model of ASD. (From BrainVTA)
The viruses used in this article from BrainVTA are in the table below
CRE Recombinase  PT-0220 rAAV-CamkII-cre-WPRE-pA
An-Ping Chai, Xue-Feng Chen, Xiao-Shan Xu, Na Zhang, Meng Li, Jin-Nan Li, Lei Zhang, Dai Zhang, Xia Zhang, Rong-Rong Mao, Yu-Qiang Ding, Lin Xu, Qi-Xin Zhou
Pub Date: 2021-06-21, DOI: 10.3389/fncel.2021.699315, Email: [email protected]
Memory-guided social recognition identifies someone from previous encounters or experiences, but the mechanisms of social memory remain unclear. Here, we find that a short-term memory from experiencing a stranger mouse lasting under 30 min interval is essential for subsequent social recognition in mice, but that interval prolonged to hours by replacing the stranger mouse with a familiar littermate. Optogenetic silencing of dorsal CA1 neuronal activity during trials or inter-trial intervals disrupted short-term memory-guided social recognition, without affecting the ability of being sociable or long-term memory-guided social recognition. Postnatal knockdown or knockout of autism spectrum disorder (ASD)-associated phosphatase and tensin homolog (PTEN) gene in dorsal hippocampal CA1 similarly impaired neuronal firing rate in vitro and altered firing pattern during social recognition. These PTEN mice showed deficits in social recognition with stranger mouse rather than littermate and exhibited impairment in T-maze spontaneous alternation task for testing short-term spatial memory. Thus, we suggest that a temporal activity of dorsal CA1 neurons may underlie formation of short-term memory to be critical for organizing subsequent social recognition but that is possibly disrupted in ASD.

Figure 1. Altered CA1 neuronal firing pattern during social recognition in conditional forebrain PTEN knockout (CKO) mice.
In this study, the authors define that a temporal activity of dorsal CA1 neurons may underlie STM for organizing social recognition but that is possibly disrupted in PTEN mouse models of ASD.
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