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J Biol Chem, Vol. 273, Issue 8, 4516-4522, February 20, 1998
§,
,, and
From the The induction of several forms of long-term
potentiation (LTP) of synaptic transmission in the CA1 region of the
mammalian hippocampus is dependent on
N-methyl-D-aspartate receptor activation and
the subsequent activation of protein kinase C (PKC), but the mechanisms
that underlie the regulation of PKC in this context are largely
unknown. It is known that reactive oxygen species, including
superoxide, are produced by
N-methyl-D-aspartate receptor activation in
neurons, and recent studies have suggested that some reactive oxygen
species can modulate PKC in vitro. Thus, we have
investigated the role of superoxide in both the induction of LTP and
the activation of PKC during LTP. We found that incubation of
hippocampal slices with superoxide scavengers inhibited the induction
of LTP. The effects of superoxide on LTP induction may involve PKC, as
we observed that superoxide was required for appropriate modulation of
PKC activation during the induction of LTP. In this respect, superoxide
appears to work in conjunction with nitric oxide, which was required
for a portion of the LTP-associated changes in PKC activity as well.
Our observations indicate that superoxide and nitric oxide together
regulate PKC in a physiologic context and that this type of regulation
occurs during the induction of LTP in the hippocampus.
Department of Neuroscience and the
§ Center for the Neural Basis of Cognition, University of
Pittsburgh, Pittsburgh, Pennsylvania 15260 and the
Division of Neuroscience, Baylor College of Medicine,
Houston, Texas 77030
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