Deficient cerebellar long-term depression, impaired eyeblink conditioning, and normal motor coordination in GFAP mutant mice

Katsuei Shibuki, Hiroshi Gomi, Lu Chen, Shaowen Bao, Jeansok J. Kim, Hidemitsu Wakatsuki, Toshiyuki Fujisaki, Kazushi Fujimoto, Akira Katoh, Toshio Ikeda, Chong Chen, Richard F. Thompson, Shigeyoshi Itohara

Research output: Contribution to journalArticlepeer-review

293 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)587-599
Number of pages13
JournalNeuron
Volume16
Issue number3
DOIs
StatePublished - Mar 1996
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)

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