Abstract
Left-right (L-R) asymmetry is a fundamental feature of brain function, but the mechanisms underlying functional asymmetry remain largely unknown. We previously identified structural and functional asymmetries in the circuitry of the mouse hippocampus that result from the asymmetrical distribution of NMDA receptor GluR ε2 (NR2B) subunits. By examining the synaptic distribution of ε2 subunits, we found that β2-microglobulin (β2m)-deficient mice that are defective in the stable cell surface expression of major histocompatibility complex class I (MHCI) lack this circuit asymmetry. To investigate the effect of hippocampal asymmetry defect on brain function, we examined working memory of β2m-deficient mice in a delayed nonmatching-to-position (DNMTP) task. Mice were trained to nosepoke either a left or right key of a sample, to retain the position of the key during a delay interval, and then to choose the key opposite from the sample. During training sessions in which no programmed delay interval was imposed, the β2m-deficient mice acquired the task as fast as control mice, suggesting that the discrimination of left and right positions is not impaired by the total loss of hippocampal asymmetry. In contrast, the β2m-deficient mice made fewer correct responses than control mice when variable delay was imposed, suggesting that the asymmetry of hippocampal circuitry plays an important role in working memory.
| Original language | English |
|---|---|
| Pages (from-to) | 50-55 |
| Number of pages | 6 |
| Journal | Neurobiology of Learning and Memory |
| Volume | 139 |
| DOIs | |
| Publication status | Published - Mar 1 2017 |
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All Science Journal Classification (ASJC) codes
- Experimental and Cognitive Psychology
- Cognitive Neuroscience
- Behavioral Neuroscience
Cite this
The asymmetry defect of hippocampal circuitry impairs working memory in β2-microglobulin deficient mice. / Goto, Kazuhiro; Ito, Isao.
In: Neurobiology of Learning and Memory, Vol. 139, 01.03.2017, p. 50-55.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The asymmetry defect of hippocampal circuitry impairs working memory in β2-microglobulin deficient mice
AU - Goto, Kazuhiro
AU - Ito, Isao
PY - 2017/3/1
Y1 - 2017/3/1
N2 - Left-right (L-R) asymmetry is a fundamental feature of brain function, but the mechanisms underlying functional asymmetry remain largely unknown. We previously identified structural and functional asymmetries in the circuitry of the mouse hippocampus that result from the asymmetrical distribution of NMDA receptor GluR ε2 (NR2B) subunits. By examining the synaptic distribution of ε2 subunits, we found that β2-microglobulin (β2m)-deficient mice that are defective in the stable cell surface expression of major histocompatibility complex class I (MHCI) lack this circuit asymmetry. To investigate the effect of hippocampal asymmetry defect on brain function, we examined working memory of β2m-deficient mice in a delayed nonmatching-to-position (DNMTP) task. Mice were trained to nosepoke either a left or right key of a sample, to retain the position of the key during a delay interval, and then to choose the key opposite from the sample. During training sessions in which no programmed delay interval was imposed, the β2m-deficient mice acquired the task as fast as control mice, suggesting that the discrimination of left and right positions is not impaired by the total loss of hippocampal asymmetry. In contrast, the β2m-deficient mice made fewer correct responses than control mice when variable delay was imposed, suggesting that the asymmetry of hippocampal circuitry plays an important role in working memory.
AB - Left-right (L-R) asymmetry is a fundamental feature of brain function, but the mechanisms underlying functional asymmetry remain largely unknown. We previously identified structural and functional asymmetries in the circuitry of the mouse hippocampus that result from the asymmetrical distribution of NMDA receptor GluR ε2 (NR2B) subunits. By examining the synaptic distribution of ε2 subunits, we found that β2-microglobulin (β2m)-deficient mice that are defective in the stable cell surface expression of major histocompatibility complex class I (MHCI) lack this circuit asymmetry. To investigate the effect of hippocampal asymmetry defect on brain function, we examined working memory of β2m-deficient mice in a delayed nonmatching-to-position (DNMTP) task. Mice were trained to nosepoke either a left or right key of a sample, to retain the position of the key during a delay interval, and then to choose the key opposite from the sample. During training sessions in which no programmed delay interval was imposed, the β2m-deficient mice acquired the task as fast as control mice, suggesting that the discrimination of left and right positions is not impaired by the total loss of hippocampal asymmetry. In contrast, the β2m-deficient mice made fewer correct responses than control mice when variable delay was imposed, suggesting that the asymmetry of hippocampal circuitry plays an important role in working memory.
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U2 - 10.1016/j.nlm.2016.12.020
DO - 10.1016/j.nlm.2016.12.020
M3 - Article
C2 - 28039089
AN - SCOPUS:85007529919
VL - 139
SP - 50
EP - 55
JO - Neurobiology of Learning and Memory
JF - Neurobiology of Learning and Memory
SN - 1074-7427
ER -