| First Author | Brown KL | Year | 2010 |
| Journal | Neurobiol Learn Mem | Volume | 93 |
| Issue | 3 | Pages | 303-11 |
| PubMed ID | 19931625 | Mgi Jnum | J:166100 |
| Mgi Id | MGI:4839705 | Doi | 10.1016/j.nlm.2009.11.004 |
| Citation | Brown KL, et al. (2010) Unimpaired trace classical eyeblink conditioning in Purkinje cell degeneration (pcd) mutant mice. Neurobiol Learn Mem 93(3):303-11 |
| abstractText | Young adult Purkinje cell degeneration (pcd) mutant mice, with complete loss of cerebellar cortical Purkinje cells, are impaired in delay eyeblink classical conditioning. In the delay paradigm, the conditioned stimulus (CS) overlaps and coterminates with the unconditioned stimulus (US), and the cerebellar cortex supports normal acquisition. The ability of pcd mutant mice to acquire trace eyeblink conditioning in which the CS and US do not overlap has not been explored. Recent evidence suggests that cerebellar cortex may not be necessary for trace eyeblink classical conditioning. Using a 500 ms trace paradigm for which forebrain structures are essential in mice, we assessed the performance of homozygous male pcd mutant mice and their littermates in acquisition and extinction. In contrast to results with delay conditioning, acquisition of trace conditioning was unimpaired in pcd mutant mice. Extinction to the CS alone did not differ between pcd and littermate control mice, and timing of the conditioned response was not altered by the absence of Purkinje cells during acquisition or extinction. The ability of pcd mutant mice to acquire and extinguish trace eyeblink conditioning at levels comparable to controls suggests that the cerebellar cortex is not a critical component of the neural circuitry underlying trace conditioning. Results indicate that the essential neural circuitry for trace eyeblink conditioning involves connectivity that bypasses cerebellar cortex. |
