The hippocampus plays an important role in eyeblink conditioning with a short trace interval in glutamate receptor subunit delta 2 mutant mice
Autor: | Shigenori Kawahara, Satoshi Fukunaga, Kanako Takatsuki, Masayoshi Mishina, Hisashi Mori, Yutaka Kirino, Sadaharu Kotani |
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Jazyk: | angličtina |
Rok vydání: | 2003 |
Předmět: |
Protein subunit
Cell Mutant Biology Hippocampal formation Brief Communication Hippocampus Cerebellar Cortex Mice medicine Hippocampus (mythology) Animals Learning Mice Knockout Behavior Animal Blinking General Neuroscience Long-Term Synaptic Depression Glutamate receptor Conditioning Eyelid Mice Inbred C57BL Kinetics medicine.anatomical_structure Eyeblink conditioning nervous system Receptors Glutamate Cerebellar cortex Mutation Neuroscience |
Zdroj: | The Journal of neuroscience : the official journal of the Society for Neuroscience = The Journal of neuroscience : the official journal of the Society for Neuroscience. 23(1):17-22 |
ISSN: | 1529-2401 |
Popis: | Mutant mice lacking the glutamate receptor subunit delta2 exhibit changes in the structure and function of the cerebellar cortex. The most prominent functional feature is a deficiency in the long-term depression (LTD) at parallel fiber-Purkinje cell synapses. These mutant mice exhibit severe impairment during delay eyeblink conditioning but learn normally during trace eyeblink conditioning without the cerebellar LTD, even with a 0 trace interval. We investigated the hippocampal contribution to this cerebellar LTD-independent "0 trace interval" learning. The mutant mice whose dorsal hippocampi were aspirated exhibited severe impairment in learning, whereas those that received post-training hippocampal lesions retained the memory. The wild-type mice showed no impairment in either case. These results suggest that the hippocampal component of the eyeblink conditioning task becomes dominant when cerebellar LTD is impaired. |
Databáze: | OpenAIRE |
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