Impaired Eye-Blink Conditioning in waggler, a Mutant Mouse With Cerebellar BDNF Deficiency

  1. Shaowen Bao,
  2. Lu Chen,
  3. Xiaoxi Qiao,
  4. Beat Knusel1, and
  5. Richard F. Thompson2
  1. Neuroscience Program, 1Andrus Gerontology Center, University of Southern California, Los Angeles, California 90089 USA

Abstract

In addition to their trophic functions, neurotrophins are also implicated in synaptic modulation and learning and memory. Although gene knockout techniques have been used widely in studying the roles of neurotrophins at molecular and cellular levels, behavioral studies using neurotrophin knockouts are limited by the early-onset lethality and various sensory deficits associated with the gene knockout mice. In the present study, we found that in a spontaneous mutant mouse, waggler, the expression of brain-derived neurotrophic factor (BDNF) was selectively absent in the cerebellar granule cells. The cytoarchitecture of the wagglercerebellum appeared to be normal at the light microscope level. The mutant mice exhibited no sensory deficits to auditory stimuli or heat-induced pain. However, they were massively impaired in classic eye-blink conditioning. These results suggest that BDNF may have a role in normal cerebellar neuronal function, which, in turn, is essential for classic eye-blink conditioning.

Footnotes

  • 2 Corresponding author.

    • Received January 26, 1998.
    • Accepted July 17, 1998.
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