Nature Neuroscience: The social novelty coding of the sea mass CA2 region and its destruction and rescue in the 22q11.2 micro-missing mouse model

Social memory is essential for a wide range of social behaviors.
social memory impairments and changes in social behavior are often associated with neuropsyurological disorders.
in humans and rodents have shown that the sea mass is not only necessary for stately memory, but also for coding social memory.
While the ability of the hema to discharge nerves (representing space, context, and semantic information) may help to remember that coding has been established, it is not clear how the hema encodes and represents social information.
the Sea Mass CA2 sub-region is a key component of the circuit necessary to encode social information into a stated memory.
social memory depends on THE projection of CA2 to the abdominal SIDE CA1, an area that is also necessary for social memory and which encodes social imprints.
, however, it is not clear whether the back-side CA2 itself encodes and how it encodes social information.
CA2 spatial discharge characteristics differ from the back-side CA1 and CA3 regions: CA2 location field has less spatial information than CA1 or CA3, and over time they are spatially unstable in the same environment, and CA2 activity is more sensitive to environmental changes than CA1 and CA3.
the role of CA2 in social memory was clinically significant, as post-mortem hema tissue in patients with schizophrenia or bipolar disorder showed a 30 percent reduction in the selectivity of neurons in CA2-positive (PV-plus).
the selective absence of CA2 in PV-intermediate neurons was also observed in the human Df (16) A-plus/- mouse model of 22q11.2 micro-missing, which increased the risk of schizophrenia by 30 times.
to determine whether CA2 activity encodes social interactions, the study recorded social behavior outside of CA2 cone neurons (PNs) cells in male mice.
although the discharge of CA2 neurons showed only weak spatial selectivity, it accurately encoded background changes and distinguished between a new and a familiar mouse.
in the human Df (16) A-plus/- mouse model, CA2 social coding was impaired, consistent with the social memory impairment observed in these mice.
, spatial coding is much more accurate.
previously found that CA2 PNs were hyperpolar in Df (16) A-plus/mice, possibly due to an increase in TREK-1 K-plus current.
paper found that TREK-1 blocking saved the social memory and CA2 social coding of Df (16) A-plus/- mice, which is supporting the key role of CA2 in the normal coding of social stimuli and the disorder of social behavioral dysfunction.
, the results of this paper further support the important role of CA2 and its dysfunction in normal social behavior and social behavior disorders in certain neuropsychiatric disorders, including schizophrenia.
addition, the findings highlight the potential importance of CA2 and TREK-1 as targets for new treatments for in-society espics associated with these diseases.
Donegan, M.L., Stefanini, F., Meira, T. et al. Coding of social novelty in the hippocampal CA2 region and its disruption and rescue in a 22q11.2 microdeletion mouse model. Nat Neurosci 23, 1365–1375 (2020). Network Source: Network Copyright Notice: All text, images and audio and video materials on this website that indicate "Source: Met Medical" or "Source: MedSci Original" are owned by Metz Medicine and are not authorized to be reproduced by any media, website or individual, and are authorized to be reproduced with the words "Source: Mets Medicine".
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