Classical eyeblink conditioning in glutamate receptor subunit δ2 mutant mice is impaired in the delay paradigm but not in the trace paradigm

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Abstract
In mice lacking glutamate receptor subunit δ2 (GluRδ2–/– 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 GluRδ2–/– 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), GluRδ2–/– 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, GluRδ2–/– 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.