Conditioned eyeblink response is impaired in mutant mice lacking NMDA receptor subunit NR2A

AUTHOR(S): Yasushi Kishimoto, Shigenori Kawahara, Yutaka Kirino, Hiroshi Kadotani, Yukihiro Nakamura, Masayuki Ikeda, Tohru Yoshioka

ABSTRACT: NMDA receptor channels, heteromeric assemblies of subunits with diverse subtypes, play critical roles in various kinds of synaptic plasticity underlying learning and memory. To elucidate the roles of subunits NR2A and NR2C in motorlearning, we investigated acquisition of the classically conditioned eyeblink response in a delayed-conditioning paradigm by gene knockout mice. Mutant mice lacking NR2C exhibited no significant defect; however, early acquisition of the task was impaired in mutant mice lacking NR2A or both NR2A and NR2C. Based on the distribution of these subunits in brain, these results indicate that acquisition of the conditioned response does not depend on NMDA receptors in the cerebellarcortex, but that its early acquisition involves the hippocampus and/or cerebellar deep nuclei.

KEYWORDS: Ca²⁺ imaging, Cerebellar deep nuclei, Cerebellum, Classical eyeblink conditioning, Gene knockout, Granule cells, Hippocampus, Long-term potentiation, Mutant mice, NMDA receptor

SUBJECT TITLE: Learning and Memory

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