Autor: | Kanako Takatsuki, Shigenori Kawahara, Sadaharu Kotani, Hisashi Mori, Masayoshi Mishina, Yutaka Kirino |
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Rok vydání: | 2002 |
Předmět: |
Neural substrate
Biophysics Glutamate receptor Hippocampus Cell Biology Hippocampal formation Biology Atomic and Molecular Physics and Optics Lesion medicine.anatomical_structure nervous system Eyeblink conditioning Cortex (anatomy) Synaptic plasticity medicine medicine.symptom Molecular Biology Neuroscience |
Zdroj: | Journal of Biological Physics. 28:539-547 |
ISSN: | 0092-0606 |
DOI: | 10.1023/a:1020362000085 |
Popis: | Cerebellar long-term depression (LTD) at the parallel fiber-Purkinje cell synapses has been proposed to be a neural substrate for classical eyeblink conditioning. Mutant mice lacking the glutamate receptor subunit δ2 (GluRδ2), in which the cerebellar LTD is disrupted, exhibited a severe impairment in the delay eyeblink conditioning with a temporal overlap of CS and US. However, they learned normally trace and delay conditioning without CS-US overlap, suggesting a learning mechanism which does not require the cerebellar LTD.In the present study, we tested possible involvement of the hippocampus in this cerebellar LTD-independent learning. We examined effects of scopolamine and hippocampal lesion on the delay conditioning without CS-US overlap. TheGluRδ2 mutant mice that received scopolamine or aspiration of the dorsalhippocampus together with its overlying cortex exhibited a severe impairment in learning, while the control mutant mice that received saline or aspiration of the overlying cortex learned normally. In contrast, wild-type mice that received either treatment learned as normally as the control wild-type mice. These results suggest that the hippocampus is essential in the cerebellar LTD-independent learning in the GluRδ2 mutant mice, indicating a newrole of hippocampus in the paradigm with a short trace interval. |
Databáze: | OpenAIRE |
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