Bilateral lesions of the interpositus nucleus completely prevent eyeblink conditioning in Purkinje cell-degeneration mutant mice.
The authors have previously demonstrated that Purkinje cell-degeneration (pcd) mutant mice are impaired in eyeblink conditioning (L. Chen et al., 1996a). The present study addresses the following 3 questions: (a) whether pcd mice perceive the conditioned and unconditioned stimuli as well as the wild-type mice, (b) whether pcd mice have a normal sensitization level, and (c) whether the residual learning in pcd mice is cerebellum-dependent. Results indicated that the pcd mice exhibited normal tone-induced responses in the cochlear nucleus and normal sensitivity to heat-induced pain. They showed a similar level of sensitization as the wild-type mice and were completely unable to learn conditioned eyeblinks after bilateral lesions aimed at the anterior interpositus nucleus. Thus, pcd mice are partially impaired in eyeblink conditioning because of a deficiency in learning mechanisms, and the residual learning in the pcd mice is mediated by the cerebellar nuclei.
Chen
L
L
Neuroscience Program, University of Southern California, Los Angeles 90089-2520, USA.
Bao
S
S
Thompson
R F
RF
D000818:Animals; D002529:Cerebellar Nuclei / Q000502:physiology*; D003214:Conditioning, Classical / Q000502:physiology*; D003215:Conditioning, Eyelid / Q000502:physiology*; D004292:Dominance, Cerebral / Q000502:physiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008818:Mice, Neurologic Mutants; D017288:Pain Threshold / Q000502:physiology; D011689:Purkinje Cells / Q000502:physiology*