Hippocampal area CA2: interneuron disfunction during pathological states

Hippocampal area CA2 plays a critical role in social recognition memory and has unique cellular and molecular properties that distinguish it from areas CA1 and CA3. In addition to having a particularly high density of interneurons, the inhibitory transmission in this region displays two distinct forms of long-term synaptic plasticity. Early studies on human hippocampal tissue have reported unique alteration in area CA2 with several pathologies and psychiatric disorders. In this review, we present recent studies revealing changes in inhibitory transmission and plasticity of area CA2 in mouse models of multiple sclerosis, autism spectrum disorder, Alzheimer's disease, schizophrenia and the 22q11.2 deletion syndrome and propose how these changes could underly deficits in social cognition observed during these pathologies.

Automated summary

The hippocampal area CA2 plays a crucial role in social recognition memory and has unique cellular and molecular properties. It has a high density of interneurons and displays two distinct forms of long-term synaptic plasticity. Recent studies have revealed changes in inhibitory transmission and plasticity of CA2 in mouse models of neurological disorders such as multiple sclerosis, autism spectrum disorder, Alzheimer's disease, schizophrenia, and the 22q11.2 deletion syndrome. These findings suggest that these changes in CA2 could contribute to the social cognitive deficits observed in these disorders.