Coding of social novelty in the hippocampal CA2 region and its disruption and rescue in a 22q11.2 microdeletion mouse model

The hippocampal CA2 region is essential for social memory. To determine whether CA2 activity encodes social interactions, we recorded extracellularly from CA2 pyramidal neurons (PNs) in male mice during social behavior. Although CA2 neuronal firing showed only weak spatial selectivity, it accurately...

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Veröffentlicht in:Nature neuroscience Jg. 23; H. 11; S. 1365 - 1375
Hauptverfasser: Donegan, Macayla L, Stefanini, Fabio, Meira, Torcato, Gordon, Joshua A, Fusi, Stefano, Siegelbaum, Steven A
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States Nature Publishing Group 01.11.2020
Schlagworte:
Action Potentials
Animals
CA2 Region, Hippocampal - physiology
Chromosome Deletion
Chromosomes, Human, Pair 22 - physiology
Coding
Disease Models, Animal
Exploratory Behavior - physiology
Hippocampus
Male
Memory
Mental disorders
Mice, Inbred C57BL
Mice, Transgenic
Neural coding
Neurons
Neurosciences
Potassium
Pyramidal cells
Pyramidal Cells - physiology
Schizophrenia
Selectivity
Social Behavior
Social factors
Social Interaction
Social interactions
Spatial Processing - physiology
ISSN:1097-6256, 1546-1726, 1546-1726
Online-Zugang:Volltext
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Zusammenfassung:The hippocampal CA2 region is essential for social memory. To determine whether CA2 activity encodes social interactions, we recorded extracellularly from CA2 pyramidal neurons (PNs) in male mice during social behavior. Although CA2 neuronal firing showed only weak spatial selectivity, it accurately encoded contextual changes and distinguished between a novel and a familiar mouse. 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. CA2 PNs were previously found to be hyperpolarized in Df(16)A mice, likely due to upregulation of TREK-1 K current. 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.
Bibliographie:ObjectType-Article-1
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ISSN:1097-6256
1546-1726
1546-1726
DOI:10.1038/s41593-020-00720-5