Memory consolidation in the cerebellar cortex

Several forms of learning, including classical conditioning of the eyeblink, depend upon the cerebellum. In examining mechanisms of eyeblink conditioning in rabbits, reversible inactivations of the control circuitry have begun to dissociate aspects of cerebellar cortical and nuclear function in memory consolidation. It was previously shown that post-training cerebellar cortical, but not nuclear, inactivations with the GABA(A) agonist muscimol prevented consolidation but these findings left open the question as to how final memory storage was partitioned across cortical and nuclear levels. Memory consolidation might be essentially cortical and directly disturbed by actions of the muscimol, or it might be nuclear, and sensitive to the raised excitability of the nuclear neurons following the loss of cortical inhibition. To resolve this question, we simultaneously inactivated cerebellar cortical lobule HVI and the anterior interpositus nucleus of rabbits during the post-training period, so protecting the nuclei from disinhibitory effects of cortical inactivation. Consolidation was impaired by these simultaneous inactivations. Because direct application of muscimol to the nuclei alone has no impact upon consolidation, we can conclude that post-training, consolidation processes and memory storage for eyeblink conditioning have critical cerebellar cortical components. The findings are consistent with a recent model that suggests the distribution of learning-related plasticity across cortical and nuclear levels is task-dependent. There can be transfer to nuclear or brainstem levels for control of high-frequency responses but learning with lower frequency response components, such as in eyeblink conditioning, remains mainly dependent upon cortical memory storage

Central effects of atropine upon aversive classical conditioning in rabbits

Rabbits were given classical discrimination conditioning with one of two tones followed by shock. In Experiment I, 40 rabbits were trained under saline, 10, 18 or 26 mg/kg atropine sulfate or 18 mg/kg methylatropine. Six rabbits in Experiment 2 were conditioned, then given further sessions with saline, and 18, 26 and 34 mg/kg atropine sulfate and methylatropine. In Experiment 3, 18 rabbits were conditioned and then given two extinction sessions under saline or 34 mg/kg atropine sulfate or methylatropine followed by extinction under saline. Chief findings were (a) atropine sulfate but not methylatropine disrupted acquisition and maintenance of conditioned eyeblinks, (b) neither drug affected unconditioned blinks, (c) fewer blinks occurred in extinction under atropine sulfate than under methylatropine or saline, (d) rabbits extinguished under atropine sulphate showed higher percentages of eyeblinks when tested without drug. Disruptions in performance of learned eyeblink responses appeared to be due to drug interference with central cholinergic transmission.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46381/1/213_2004_Article_BF00406735.pd