Neural substrates of eyeblink conditioning: acquisition and retention.
In well-trained animals, infusion of the GABA-B agonist baclofen into the cerebellar interpositus nucleus and overlying cortex abolished the conditioned response (CR) with no effect on the unconditioned response (UR) with doses at or above 5.0 mM. Infusion of the GABA-B antagonist CGP 5584-5A alone had no effect on the CR or UR. However, administration of 5 mM baclofen soon after infusion of CGP 5584-5A (15 min) resulted in no reduction of percent CR and only partial reduction of CR amplitude. Naive animals given interpositus infusions of baclofen during training showed no learning, yet learned normally in postinfusion training. The distribution of (radiolabelled) baclofen was localized and remained within the cerebellum. The results presented here are consistent with a growing body of literature supporting the hypothesis that the memory trace for eyeblink conditioning is formed and stored in the cerebellum and may involve GABAergic mechanisms.