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(Received for publication, June 26, 1996, and in revised form, September 3, 1996)
From the Division of Neuroscience, Baylor College of Medicine,
Houston, Texas 77030-3498
Long-term potentiation (LTP) in the hippocampus
is a possible mechanism for mammalian learning and memory in which
protein kinases play critical roles. We have investigated the
involvement of cyclic AMP-dependent protein kinase (PKA) in
LTP by directly studying its activation. We developed an in
vitro assay which is useful for selective and accurate
measurement of stimulus-induced changes in PKA activity in hippocampal
slices. PKA was transiently activated 2 and 10 min after delivery of
LTP-inducing stimuli in area CA1 of the hippocampus. This activation
did not persist during early or late phases of LTP, suggesting that the
role of PKA is in the induction of LTP, not in its expression. LTP was not associated with any change in the total activity of PKA, consistent with activation by cyclic AMP, as opposed to an increase in the amount
or efficacy of the enzyme. The LTP-associated activation of PKA
required stimulation of the
N-methyl-D-aspartate (NMDA) subtype of
glutamate receptor, and bath application of NMDA was sufficient to
activate PKA. Together, these results indicate that at the initiation
of LTP, NMDA receptor stimulation leads to transient activation of PKA,
and support a role for PKA in the induction of LTP.
Volume 271, Number 48,
Issue of November 29, 1996
pp. 30436-30441
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
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