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Journal of Neuroscience, Vol 12, 4403-4426, Copyright © 1992 by Society for Neuroscience
Disruption of classical eyelid conditioning after cerebellar lesions: damage to a memory trace system or a simple performance deficit?
JE Steinmetz, DG Lavond, D Ivkovich, CG Logan and RF Thompson
Department of Psychology, Indiana University, Bloomington 47405.
Over the past 10 years, a number of laboratories have reported that
classically conditioned skeletal muscle responses, such as conditioned
nictitating membrane/eyelid responses, are critically dependent on activity
in the cerebellum. For example, unilateral lesions of the cerebellar
interpositus nucleus have been shown to prevent acquisition and abolish
retention of the conditioned eyelid response on the side ipsilateral to the
lesions without affecting conditioned responding (CR) on the contralateral
side. Also, recording studies involving the interpositus nucleus have
consistently revealed patterns of neuronal discharge that predict execution
of the CR. The lesion and recording studies have generally been cited as
evidence that plasticity in the cerebellum is critically involved in the
learning and memory of classically conditioned responses. This
interpretation was recently challenged by Welsh and Harvey (1989a), who
claimed that cerebellar lesions simply produced a performance deficit and
speculated that the role of the cerebellum was not in learning and memory
processes associated with the CR but only in performance of the eye blink
response. Presented here are three experiments that provide additional
strong evidence for a critical role of the cerebellum in the learning and
memory of the Pavlovian CR. These experiments include (1) demonstrations of
complete and permanent CR abolition after appropriate interpositus lesions,
(2) a failure to find systematic or persisting decrements in the
unconditioned response amplitude (i.e., the eye blink reflex) after
appropriate interpositus lesion, and (3) observations of differential
effects on the CR and unconditioned response after lesions were placed in
populations of motoneurons responsible for executing the eye blink
response. These data are discussed in the context of performance versus
learning issues; evidence presented here rules out the possibility that
interpositus lesion abolition of the eye blink CR is simply due to lesion
effects on performance.
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