TY - JOUR
T1 - Deficient cerebellar long-term depression, impaired eyeblink conditioning, and normal motor coordination in GFAP mutant mice
AU - Shibuki, Katsuei
AU - Gomi, Hiroshi
AU - Chen, Lu
AU - Bao, Shaowen
AU - Kim, Jeansok J.
AU - Wakatsuki, Hidemitsu
AU - Fujisaki, Toshiyuki
AU - Fujimoto, Kazushi
AU - Katoh, Akira
AU - Ikeda, Toshio
AU - Chen, Chong
AU - Thompson, Richard F.
AU - Itohara, Shigeyoshi
N1 - Funding Information:
We wish to thank all the members of the Itohara lab for their encouragement, and for maintaining mice; T. Kaneko, A. Aiba, and H. Ohishi for their helpful discussions, and T. Hirano and A. Silva for their comments on the manuscripts. We wish to thank K. Mikoshiba, S. Nakanishi, and A. Aiba for providing monoclonal antibody to IP 3 R1, polyclonal antibodies to mGluR1, and mGluR1-deficient mice, respectively. H. G., T.I., S. I., and C. C. wish to thank S. Tonegawa for his invaluable help and continuous encouragement. This work was supported by grants from the Shionogi Institute for Medical Science, the Japanese Ministry of Education, Science, and Culture, and Japanese Ministry of Public Welfare to S. I.; grants from Japanese Ministry of Education, Science, and Culture, Japanese Ministry of Public Welfare, Uehara Memorial Foundation, Toyota RIKEN, and Nissan Science foundation to K. S., grants from the Howard Hughes Medical Institute to C. C.; and grants from the National Science Foundation, the National Institute on Aging, and Sankyo to R. F. T.
PY - 1996/3
Y1 - 1996/3
N2 - Mice devoid of glial fibrillary acidic protein (GFAP), an intermediate filament protein specifically expressed in astrocytes, develop normally and do not show any detectable abnormalities in the anatomy of the brain. In the cerebellum, excitatory synaptic transmission from parallel fibers (PFs) or climbing fibers (CFs) to Purkinje cells is unaltered, and these synapses display normal short-term synaptic plasticity to paired stimuli in GFAP mutant mice. In contrast, long-term depression (LTD) at PF-Purkinje cell synapses is clearly deficient. Furthermore, GFAP mutant mice exhibited a significant impairment of eyeblink conditioning without any detectable deficits in motor coordination tasks. These results suggest that GFAP is required for communications between Bergmann glia and Purkinje cells during LTD induction and maintenance. The data support the notion that cerebellar LTD is a cellular mechanism closely associated with eyeblink conditioning, but is not essential for motor coordination tasks tested.
AB - Mice devoid of glial fibrillary acidic protein (GFAP), an intermediate filament protein specifically expressed in astrocytes, develop normally and do not show any detectable abnormalities in the anatomy of the brain. In the cerebellum, excitatory synaptic transmission from parallel fibers (PFs) or climbing fibers (CFs) to Purkinje cells is unaltered, and these synapses display normal short-term synaptic plasticity to paired stimuli in GFAP mutant mice. In contrast, long-term depression (LTD) at PF-Purkinje cell synapses is clearly deficient. Furthermore, GFAP mutant mice exhibited a significant impairment of eyeblink conditioning without any detectable deficits in motor coordination tasks. These results suggest that GFAP is required for communications between Bergmann glia and Purkinje cells during LTD induction and maintenance. The data support the notion that cerebellar LTD is a cellular mechanism closely associated with eyeblink conditioning, but is not essential for motor coordination tasks tested.
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U2 - 10.1016/S0896-6273(00)80078-1
DO - 10.1016/S0896-6273(00)80078-1
M3 - Article
C2 - 8785056
AN - SCOPUS:13344269673
SN - 0896-6273
VL - 16
SP - 587
EP - 599
JO - Neuron
JF - Neuron
IS - 3
ER -