Bilateral lesions of the interpositus nucleus completely prevent eyeblink conditioning in purkinje cell-degeneration mutant mice

Lu Chen, Shaowen Bao, Richard F. Thompson

Research output: Contribution to journalArticlepeer-review

50 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)204-210
Number of pages7
JournalBehavioral Neuroscience
Volume113
Issue number1
DOIs
StatePublished - 1999
Externally publishedYes

ASJC Scopus subject areas

  • Behavioral Neuroscience

Fingerprint

Dive into the research topics of 'Bilateral lesions of the interpositus nucleus completely prevent eyeblink conditioning in purkinje cell-degeneration mutant mice'. Together they form a unique fingerprint.

Cite this