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A weakened recurrent circuit in the hippocampus of Rett syndrome mice disrupts long-term memory representations


Authors: Lingjie He, Matthew S. Caudill, Junzhan Jing, Wei Wang, Yaling Sun, Jianrong Tang, Xiaolong Jiang, Huda Y. Zoghbi
Publication: Neuron
Date: May 18, 2022
Link to article: https://doi.org/10.1016/j.neuron.2022.02.014


Successful recall of a contextual memory requires reactivating ensembles of hippocampal cells that were allocated during memory formation. Altering the ratio of excitation-to-inhibition (E/I) during memory retrieval can bias cell participation in an ensemble and hinder memory recall. In the case of Rett syndrome (RTT), a neurological disorder with severe learning and memory deficits, the E/I balance is altered, but the source of this imbalance is unknown. Using in vivo imaging during an associative memory task, we show that during long-term memory retrieval, RTT CA1 cells poorly distinguish mnemonic context and form larger ensembles than wild-type mouse cells. Simultaneous multiple whole-cell recordings revealed that mutant somatostatin expressing interneurons (SOM) are poorly recruited by CA1 pyramidal cells and are less active during long-term memory retrieval in vivo. Chemogenetic manipulation revealed that reduced SOM activity underlies poor long-term memory recall. Our findings reveal a disrupted recurrent CA1 circuit contributing to RTT memory impairment.

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