DEFICIENT CEREBELLAR LONG-TERM DEPRESSION, IMPAIRED EYEBLINK CONDITIONING, AND NORMAL MOTOR COORDINATION IN GFAP MUTANT MICE

Mice devoid of glial fibrillary acidic protein (GFAP), an intermediate filament protein specifically expressed in astrocytes, develop normal ly and do not show any detectable abnormalities in the anatomy of the brain. In the cerebellum, excitatory synaptic transmission from parall el fibers (PFs) or climbing fibers (CFs) to Purkinje cells is unaltere d, 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 condi tioning without any detectable deficits in motor coordination tasks. T hese 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 mechani sm closely associated with eyeblink conditioning, but is not essential for motor coordination tasks tested.