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Long‐trace interval eyeblink conditioning is impaired in mutant mice lacking the NMDA receptor subunit ε1
Author(s) -
Kishimoto Yasushi,
Kawahara Shigenori,
Mori Hisashi,
Mishina Masayoshi,
Kirino Yutaka
Publication year - 2001
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.0953-816x.2001.01486.x
Subject(s) - eyeblink conditioning , nmda receptor , conditioning , neuroscience , associative learning , protein subunit , hippocampus , chemistry , mutant , glutamate receptor , long term potentiation , classical conditioning , psychology , receptor , biochemistry , mathematics , statistics , gene
To elucidate the role of the N ‐methyl‐ d ‐aspartate (NMDA) ‐type glutamate receptor subunit ε1 (GluRε1) in classical eyeblink conditioning, delay and trace eyeblink conditioning were investigated in GluRε1‐null mutant mice. In delay conditioning and short‐trace interval conditioning with a trace interval of 250 ms, GluRε1 mutant mice attained a normal level of the conditioned response (CR), although acquisition was a little slower than in wild‐type mice. In contrast, GluRε1 mutant mice exhibited severe impairment of the attained level of the CR and disturbed temporal pattern of CR expression in trace conditioning with a longer trace interval of 500 ms. These findings indicate that GluRε1 is essential for long‐trace interval eyeblink conditioning. The impairments of the associative learning with a long temporal separation between the conditioned and unconditioned stimuli observed in the GluRε1 mutant mice could be attributed to an impairment of hippocampal long‐term potentiation in this line of mutant mice.