Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9415789 | Brain Research | 2005 | 9 Pages |
Abstract
We have shown that glutamate receptor subunit δ2 (GluRδ2) null mutant mice, which have serious morphological and functional deficiencies in the cerebellar cortex, are severely impaired in delay eyeblink conditioning but not in trace eyeblink conditioning, even with a 0-trace interval. Such 0-trace conditioning does not depend critically on the hippocampus in wild-type mice, but it does in GluRδ2 mutant mice. Here we examined the hippocampal electroencephalogram (EEG) during 0-trace conditioning in GluRδ2 mutant and wild-type mice. During the apparatus habituation sessions, the total hippocampal theta activity (4-12 Hz) of GluRδ2 mutant mice was less than that of wild-type mice. Activity in the higher frequency band (8-12 Hz, type 1) in GluRδ2 mutant mice was significantly less than it was in wild-type mice, but activity in the lower frequency band (4-8 Hz, type 2) was not. As learning proceeded during the acquisition sessions, the total theta activity decreased in many of the wild-type mice, while this phenomenon was less prominent in GluRδ2 mutant mice. Further analysis showed that the type 1 activity in wild-type mice increased in the early sessions and then decreased, while that in GluRδ2 mutant mice did not change. Type 2 activity tended to decrease in both types of mice as the conditioning proceeded. These results indicate that the distribution of hippocampal EEG frequency and its properties during conditioning are different between wild-type and GluRδ2 mutant mice, suggesting that the cerebellar cortical dysfunction may cause an alteration in the electrophysiological characteristics of the hippocampus.
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Authors
Kanako Takatsuki, Shigenori Kawahara, Masayoshi Mishina, Yutaka Kirino,