| First Author | Goto K | Year | 2017 |
| Journal | Neurobiol Learn Mem | Volume | 139 |
| Pages | 50-55 | PubMed ID | 28039089 |
| Mgi Jnum | J:273761 | Mgi Id | MGI:6282493 |
| Doi | 10.1016/j.nlm.2016.12.020 | Citation | Goto K, et al. (2017) The asymmetry defect of hippocampal circuitry impairs working memory in beta2-microglobulin deficient mice. Neurobiol Learn Mem 139:50-55 |
| abstractText | 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 epsilon2 (NR2B) subunits. By examining the synaptic distribution of epsilon2 subunits, we found that beta2-microglobulin (beta2m)-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 beta2m-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 beta2m-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 beta2m-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. |
