| First Author | He L | Year | 2022 |
| Journal | Neuron | Volume | 110 |
| Issue | 10 | Pages | 1689-1699.e6 |
| PubMed ID | 35290792 | Mgi Jnum | J:326152 |
| Mgi Id | MGI:7294117 | Doi | 10.1016/j.neuron.2022.02.014 |
| Citation | He L, et al. (2022) A weakened recurrent circuit in the hippocampus of Rett syndrome mice disrupts long-term memory representations. Neuron 110(10):1689-1699.e6 |
| abstractText | 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. |
