| First Author | Takatsuki K | Year | 2003 |
| Journal | J Neurosci | Volume | 23 |
| Issue | 1 | Pages | 17-22 |
| PubMed ID | 12514196 | Mgi Jnum | J:124824 |
| Mgi Id | MGI:3722576 | Doi | 10.1523/JNEUROSCI.23-01-00017.2003 |
| Citation | Takatsuki K, et al. (2003) The hippocampus plays an important role in eyeblink conditioning with a short trace interval in glutamate receptor subunit delta 2 mutant mice. J Neurosci 23(1):17-22 |
| abstractText | Mutant mice lacking the glutamate receptor subunit delta2 exhibit changes in the structure and function of the cerebellar cortex. The most prominent functional feature is a deficiency in the long-term depression (LTD) at parallel fiber-Purkinje cell synapses. These mutant mice exhibit severe impairment during delay eyeblink conditioning but learn normally during trace eyeblink conditioning without the cerebellar LTD, even with a 0 trace interval. We investigated the hippocampal contribution to this cerebellar LTD-independent '0 trace interval' learning. The mutant mice whose dorsal hippocampi were aspirated exhibited severe impairment in learning, whereas those that received post-training hippocampal lesions retained the memory. The wild-type mice showed no impairment in either case. These results suggest that the hippocampal component of the eyeblink conditioning task becomes dominant when cerebellar LTD is impaired. |
