| First Author | Kishimoto Y | Year | 2001 |
| Journal | Eur J Neurosci | Volume | 13 |
| Issue | 6 | Pages | 1249-53 |
| PubMed ID | 11285022 | Mgi Jnum | J:89436 |
| Mgi Id | MGI:3040150 | Doi | 10.1046/j.0953-816x.2001.01488.x |
| Citation | Kishimoto Y, et al. (2001) Classical eyeblink conditioning in glutamate receptor subunit delta 2 mutant mice is impaired in the delay paradigm but not in the trace paradigm. Eur J Neurosci 13(6):1249-53 |
| abstractText | In mice lacking glutamate receptor subunit delta 2 (GluR delta 2(-/-_ mice), cerebellar long-term depression (LTD) at the parallel fibre-Purkinje cell synapses is disrupted. Unlike the cerebellar LTD-deficient mice previously used for eyeblink conditioning, however, the abnormalities of the GluR delta 2(-/-) mice are restricted to the cerebellar cortex. In delay eyeblink conditionings (interstimulus interval of 252 and 852 ms), in which the conditioned stimulus (CS) overlaps temporally with a coterminating unconditioned stimulus (US), GluR delta 2(-/-) mice are severely impaired in learning, strongly supporting the hypothesis that cerebellar cortical LTD is essential for delay conditioning. In the trace paradigm, in which a stimulus-free trace interval of 500 ms intervened between the CS and US, GluR delta 2(-/-) mice learned as successfully as wild-type mice, indicating that cerebellar LTD is not necessary for trace conditioning. Thus, the present study has revealed a cerebellar LTD-independent learning in eyeblink conditioning. |
