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Classical eyeblink conditioning in glutamate receptor subunit δ2 mutant mice is impaired in the delay paradigm but not in the trace paradigm
Author(s) -
Kishimoto Yasushi,
Kawahara Shigenori,
Suzuki Michiyuki,
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.2001.01488.x
Subject(s) - eyeblink conditioning , neuroscience , classical conditioning , cerebellum , interstimulus interval , psychology , cerebellar cortex , conditioning , purkinje cell , glutamate receptor , chemistry , receptor , stimulation , biochemistry , statistics , mathematics
In mice lacking glutamate receptor subunit δ2 (GluRδ2 –/– mice), cerebellar long‐term depression (LTD) at the parallel fibre–Purkinje cell synapses is disrupted. Unlike the cerebellar LTD‐deficient mice previously used for eyeblink conditioning, however, the abnormalities of the GluRδ2 –/– mice are restricted to the cerebellar cortex. In delay eyeblink conditionings (interstimulus interval of 252 and 852 ms), in which the conditioned stimulus (CS) overlaps temporally with a coterminating unconditioned stimulus (US), GluRδ2 –/– mice are severely impaired in learning, strongly supporting the hypothesis that cerebellar cortical LTD is essential for delay conditioning. In the trace paradigm, in which a stimulus‐free trace interval of 500 ms intervened between the CS and US, GluRδ2 –/– mice learned as successfully as wild‐type mice, indicating that cerebellar LTD is not necessary for trace conditioning. Thus, the present study has revealed a cerebellar LTD‐independent learning in eyeblink conditioning.