| First Author | Chen L | Year | 1999 |
| Journal | Behav Neurosci | Volume | 113 |
| Issue | 1 | Pages | 204-10 |
| PubMed ID | 10197920 | Mgi Jnum | J:54145 |
| Mgi Id | MGI:1334143 | Doi | 10.1037//0735-7044.113.1.204 |
| Citation | Chen L, et al. (1999) Bilateral lesions of the interpositus nucleus completely prevent eyeblink conditioning in Purkinje cell-degeneration mutant mice. Behav Neurosci 113(1):204-10 |
| abstractText | 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 an 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. |
