Brain, Vol 120, Issue 8 1401-1413, Copyright © 1997 by Oxford University Press
V Bracha, L Zhao, DA Wunderlich, SJ Morrissy and JR Bloedel
The purpose of these experiments was to examine the role of the human
cerebellum in the acquisition and retention of conditioned reflexes. Normal
human subjects and patients with cerebellar lesions were tested for their
capacity to acquire, retain and express conditioned eyeblink responses. In
acquisition tests, subjects were trained in a delay classical conditioning
paradigm using a tone conditioned stimulus and a midline forehead tap as an
unconditioned stimulus. While normal subjects developed anticipatory
eyeblinks to the tone in one session, patients with cerebellar lesions
failed to acquire conditioned responses in four consecutive training
sessions. The conditioning deficit was bilateral even in patients with a
unilateral cerebellar pathology. The same groups of subjects were tested
for the presence of eyeblinks to a visual threat. In these experiments,
both normal subjects and patients with cerebellar lesions exhibited a high
level of responding when they saw an object approaching their face. These
eyeblinks to the visual threat are probably naturally acquired conditioned
responses because they extinguish in normal subjects if they are not
reinforced by the unconditioned cutaneous stimulus. In addition, the
stimulus of seeing an approaching object blocks the acquisition of
classically conditioned eyeblinks to a new conditioned stimulus in normal
subjects. These data imply that patients with cerebellar lesions who cannot
acquire new classically conditioned responses are able to retain and
express conditioned eyeblinks which were acquired before the onset of the
pathology. Consequently, cerebellum-dependent neural substrates which are
involved in learning new conditioned reflexes do not seem to be required
for the storage of naturally learned conditioned responses.
ARTICLES
Patients with cerebellar lesions cannot acquire but are able to retain conditioned eyeblink reflexes
Division of Neurobiology, Barrow Neurological Institute, Phoenix, AZ 85013, USA.
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