![]() Chronic loss of CA2 transmission leads to hippocampal hyperexcitability. CNS distribution of members of the two-pore-domain (KCNK) potassium channel family. 22q11.2 microdeletions: linking DNA structural variation to brain dysfunction and schizophrenia. Age-dependent specific changes in area CA2 of the hippocampus and social memory deficit in a mouse model of the 22q11.2 deletion syndrome. A selective decrease in the relative density of parvalbumin- immunoreactive neurons in the hippocampus in schizophrenia. A reduction of nonpyramidal cells in sector CA2 of schizophrenics and manic depressives. The hippocampal CA2 ensemble is sensitive to contextual change. Topography of place maps along the CA3-to-CA2 axis of the hippocampus. Spatial coding and physiological properties of hippocampal neurons in the Cornu Ammonis subregions. Social and novel contexts modify hippocampal CA2 representations of space. Hippocampal CA2 activity patterns change over time to a larger extent than between spatial contexts. Neuronal responses to conspecifics in the ventral CA1. Lesions to the CA2 region of the hippocampus impair social memory in mice. The hippocampal CA2 region is essential for social memory. A hippocampal circuit linking dorsal CA2 to ventral CA1 critical for social memory dynamics. Hippocampal representation of related and opposing memories develop within distinct, hierarchically organized neural schemas. Hippocampal ‘time cells’: time versus path integration. Kraus, B., Robinson, R., White, J., Eichenbaum, H. Hippocampal ‘time cells’ bridge the gap in memory for discontiguous events. Preliminary evidence from unit activity in the freely-moving rat. The cognitive neuroscience of human memory since H. Long-term memory underlying hippocampus- dependent social recognition in mice. Medial temporal lobe structures are needed to re-experience remote autobiographical memories: evidence from H. Neuropsychologic deficits in schizophrenia: relation to social function and effect of antipsychotic drug treatment. Life history and bioeconomy of the house mouse. 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.īerry, R. CA2 PNs were previously found to be hyperpolarized in Df(16)A +/− mice, likely due to upregulation of TREK-1 K + current. 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. Although CA2 neuronal firing showed only weak spatial selectivity, it accurately encoded contextual changes and distinguished between a novel and a familiar mouse. To determine whether CA2 activity encodes social interactions, we recorded extracellularly from CA2 pyramidal neurons (PNs) in male mice during social behavior.
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