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Journal of Neuroscience, Vol 10, 2300-2307, Copyright © 1990 by Society for Neuroscience
Regulation of short-term associative memory by calcium-dependent protein kinase
LD Matzel, II Lederhendler and DL Alkon
Section on Neural Systems, National Institutes of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892.
Neural and behavioral correlates of an associative memory in Hermissenda
were examined during induction and/or formation of the memory. Hermissenda
received either light (conditioned stimulus or CS) and rotation
(unconditioned stimulus or US) paired (i.e., Pavlovian conditioning), light
and rotation unpaired (pseudoconditioning), or no exposure to light and
rotation. Following 9 pairings in a 6 min session, conditioned animals
exhibited a contraction of the foot in response to a test CS presented 2
min after the last conditioning trial, whereas pseudoconditioned and
untreated animals exhibited a foot extension to the same CS. In addition,
both an associative and a nonassociative reduction in light-induced
locomotion was observed. To examine neural correlates of this learning
within minutes of acquisition, the isolated nervous system of the
Hermissenda (containing the visual and vestibular organs) was trained with
stimulus conditions identical to those used for the intact animal. Prior
isolation and preparation of the nervous system permitted immediate
intracellular recording following the final conditioning trial. Relative to
pseudoconditioned and untreated animals, the B photoreceptors in
conditioned nervous systems were found to have elevated input resistance
(inversely related to K+ channel conductance and positively related to
excitability) and exhibited increased steady-state depolarization in
response to the light CS, as well as a prolonged depolarization after the
CS offset. These neural correlates of the associative memory were
attenuated if the protein kinase inhibitor H7 was present in the
extracellular bath during conditioning, demonstrating in the reduced
preparation that antagonism of protein kinase activity blocks the induction
of membrane alterations of identified neurons that correlate with memory
storage.(ABSTRACT TRUNCATED AT 250 WORDS)
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