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J. Biol. Chem., Vol. 266, Issue 36, 24253-24256, Dec, 1991
E Klann, SJ Chen and JD Sweatt
Long-term potentiation (LTP) of synaptic transmission in the hippocampus is
a robust form of synaptic plasticity that may contribute to mammalian
memory formation. A variety of pharmacological evidence suggests that
persistent kinase activation contributes to the maintenance of LTP. To
determine whether persistent activation of protein kinases was associated
with the maintenance phase of LTP, protein kinase activity was measured in
control and LTP samples using exogenous protein kinase substrates in an in
vitro assay of homogenates of the CA1 region of rat hippocampal slices.
After LTP, protein kinase activity was persistently increased, and the
induction of this effect was blocked by the N-methyl-D-aspartate receptor
antagonist DL-2-amino- 5-phosphonovaleric acid. The increased protein
kinase activity was found to be significantly attenuated by PKC(19-36), a
selective peptide inhibitor of protein kinase C. Thus, LTP is associated
with an N-methyl- D-aspartate receptor-mediated generation of a
persistently activated form of protein kinase C. These data lend strong
support to the model that persistent protein kinase activation contributes
to the maintenance of LTP.
Persistent protein kinase activation in the maintenance phase of long- term potentiation
Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030.
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