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

First Author  Kishimoto Y Year  1997
Journal  Neuroreport Volume  8
Issue  17 Pages  3717-21
PubMed ID  9427357 Mgi Jnum  J:103735
Mgi Id  MGI:3610666 Doi  10.1097/00001756-199712010-00012
Citation  Kishimoto Y, et al. (1997) Conditioned eyeblink response is impaired in mutant mice lacking NMDA receptor subunit NR2A. Neuroreport 8(17):3717-21
abstractText  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 motor learning, 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 cerebellar cortex, but that its early acquisition involves the hippocampus and/or cerebellar deep nuclei.
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