Abstract
Social recognition memory is crucial for survival across species, underlying the need to correctly identify conspecifics, mates and potential enemies. In humans the hippocampus is engaged in social and episodic memory, however the circuit mechanisms of social memory in rodent models has only recently come under scrutiny. Work in mice has established that the dorsal CA2 and ventral CA1 regions play critical roles, however a more comprehensive comparative analyses of the circuits and mechanisms required has not been reported. Here we employ conditional genetics to examine the differential contributions of the hippocampal subfields to social memory. We find that the deletion of NMDA receptor subunit 1 gene (NR1), which abolishes NMDA receptor synaptic plasticity, in CA3 pyramidal cells led to deficits in social memory; however, mice lacking the same gene in DG granule cells performed indistinguishable from controls. Further, we use conditional pharmacogenetic inhibition to demonstrate that activity in ventral, but not dorsal, CA3 is necessary for the encoding of a social memory. These findings demonstrated CA3 pyramidal cell plasticity and transmission contribute to the encoding of social stimuli and help further identify the distinct circuits underlying the role of the hippocampus in social memory.
| Original language | English |
|---|---|
| Journal | Behavioural Brain Research |
| DOIs | |
| Publication status | Accepted/In press - 2018 Jan 1 |
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Keywords
- CA3
- Hippocampus
- Social memory
- Synaptic plasticity
ASJC Scopus subject areas
- Behavioral Neuroscience
Cite this
A role for CA3 in social recognition memory. / Chiang, Ming Ching; Huang, Arthur J.Y.; Wintzer, Marie E.; Ohshima, Toshio; McHugh, Thomas J.
In: Behavioural Brain Research, 01.01.2018.Research output: Contribution to journal › Article
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TY - JOUR
T1 - A role for CA3 in social recognition memory
AU - Chiang, Ming Ching
AU - Huang, Arthur J.Y.
AU - Wintzer, Marie E.
AU - Ohshima, Toshio
AU - McHugh, Thomas J.
PY - 2018/1/1
Y1 - 2018/1/1
N2 - Social recognition memory is crucial for survival across species, underlying the need to correctly identify conspecifics, mates and potential enemies. In humans the hippocampus is engaged in social and episodic memory, however the circuit mechanisms of social memory in rodent models has only recently come under scrutiny. Work in mice has established that the dorsal CA2 and ventral CA1 regions play critical roles, however a more comprehensive comparative analyses of the circuits and mechanisms required has not been reported. Here we employ conditional genetics to examine the differential contributions of the hippocampal subfields to social memory. We find that the deletion of NMDA receptor subunit 1 gene (NR1), which abolishes NMDA receptor synaptic plasticity, in CA3 pyramidal cells led to deficits in social memory; however, mice lacking the same gene in DG granule cells performed indistinguishable from controls. Further, we use conditional pharmacogenetic inhibition to demonstrate that activity in ventral, but not dorsal, CA3 is necessary for the encoding of a social memory. These findings demonstrated CA3 pyramidal cell plasticity and transmission contribute to the encoding of social stimuli and help further identify the distinct circuits underlying the role of the hippocampus in social memory.
AB - Social recognition memory is crucial for survival across species, underlying the need to correctly identify conspecifics, mates and potential enemies. In humans the hippocampus is engaged in social and episodic memory, however the circuit mechanisms of social memory in rodent models has only recently come under scrutiny. Work in mice has established that the dorsal CA2 and ventral CA1 regions play critical roles, however a more comprehensive comparative analyses of the circuits and mechanisms required has not been reported. Here we employ conditional genetics to examine the differential contributions of the hippocampal subfields to social memory. We find that the deletion of NMDA receptor subunit 1 gene (NR1), which abolishes NMDA receptor synaptic plasticity, in CA3 pyramidal cells led to deficits in social memory; however, mice lacking the same gene in DG granule cells performed indistinguishable from controls. Further, we use conditional pharmacogenetic inhibition to demonstrate that activity in ventral, but not dorsal, CA3 is necessary for the encoding of a social memory. These findings demonstrated CA3 pyramidal cell plasticity and transmission contribute to the encoding of social stimuli and help further identify the distinct circuits underlying the role of the hippocampus in social memory.
KW - CA3
KW - Hippocampus
KW - Social memory
KW - Synaptic plasticity
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UR - http://www.scopus.com/inward/citedby.url?scp=85041616953&partnerID=8YFLogxK
U2 - 10.1016/j.bbr.2018.01.019
DO - 10.1016/j.bbr.2018.01.019
M3 - Article
C2 - 29355673
AN - SCOPUS:85041616953
JO - Behavioural Brain Research
JF - Behavioural Brain Research
SN - 0166-4328
ER -