Compensatory Mechanisms at the Level of the Vestibular Nuclei Following Post-Natal Degeneration of Specific Cerebellar Cell Classes and Ablation of the Cerebellum in Mutant Mice

  • U. Grüsser-Cornehls


Neurological diseases with genetic cerebellar defects play a not inconsiderable role in human medicine (Gilman et al. 1981). Differentiation and treatment and the exploration of the dynamic pathophysiological processes, e.g., the degenerative processes and the resulting compensation mechanisms, are to date still very unsatisfactory. Mutant mice with cerebellar degenerative defects (Sidman et al. 1965; Herrup and Mullen 1979) may advance our understanding in such diseases by providing a tool for investigating the neurophysiological and neuroanatomical bases of behavioral deficiencies and compensation mechanisms resulting from a particular lesion, the loss of a single or a restricted number of nerve cell classes. For this reason, neuroanatomical (Grover and Grüsser-Cornehls 1976), electrophysiological (Grüsser-Cornehls 1983; Helmchen et al. 1985), synaptic transmitter (Kahle and Grüsser-Cornehls 1987) and immunohistochemical investigations were undertaken in two “extreme” specimens of these mutant mice: the Weaver mice and the Purkinje cell degeneration (pcd) mice.


Mutant Mouse Vestibular Nucleus Vestibular Stimulation Vestibular Neuron Nucleus Interpositus 
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Copyright information

© Springer-Verlag Berlin Heidelberg 1988

Authors and Affiliations

  • U. Grüsser-Cornehls
    • 1
  1. 1.Department of PhysiologyFreie Universität BerlinBerlin (West) 33Germany

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