Long‐trace interval eyeblink conditioning is impaired in mutant mice lacking the NMDA receptor subunit ε1

• Yasushi Kishimoto

• Shigenori Kawahara

• Hisashi Mori

• Masayoshi Mishina

• Yutaka Kirino

抄録

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.

収録刊行物

• European Journal of Neuroscience

  European Journal of Neuroscience 13 (6), 1221-1227, 2001-03

  Wiley

キーワード

• General Neuroscience

詳細情報

• CRID: 1360574093745298176
• NII論文ID: 30014382011
• DOI: 10.1046/j.0953-816x.2001.01486.x
• ISSN: 14609568
• ISSN: 0953816X
• Web Site: https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1046%2Fj.0953-816x.2001.01486.x
• Web Site: https://onlinelibrary.wiley.com/doi/pdf/10.1046/j.0953-816x.2001.01486.x
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