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Journal of Neuroscience, Vol 7, 3675-3686, Copyright © 1987 by Society for Neuroscience
Metabolites of arachidonic acid in the nervous system of Aplysia: possible mediators of synaptic modulation
D Piomelli, E Shapiro, SJ Feinmark and JH Schwartz
Department of Pharmacology, Columbia University, New York, New York 10032.
Release of arachidonic acid from membrane phospholipids is receptor-
mediated and might generate second messengers in neurons. We tested this
idea using the simple nervous system of the marine mollusk, Aplysia
californica. Aplysia neural components metabolize arachidonic acid through
lipoxygenase and cyclo-oxygenase pathways. We identified 2 major
lipoxygenase products, 12- and 5-hydroxyeicosatetraenoic acids (12-HETE and
5-HETE), and 2 cyclo-oxygenase products, PGE2 and PGF2 alpha. These
metabolites of arachidonic acid are formed in synaptosomes, as well as in
identified nerve cell bodies, indicating that both lipoxygenase and
cyclo-oxygenase pathways are active within neurons. Application of the
modulatory neurotransmitter histamine to cerebral ganglia that had been
labeled with 3H-arachidonic acid induced the formation of 3H-12-HETE. This
response was inhibited by the histamine antagonist cimetidine. Furthermore,
release of radioactive 5- HETE and 12-HETE was observed after intracellular
stimulation of the histaminergic cell C2 in cerebral ganglia labeled with
3H-arachidonic acid. Cimetidine also inhibited this response. Application
of serotonin or stimulation of the giant serotonergic cell (GCN) in the
cerebral ganglion did not cause detectable amounts of the labeled
eicosanoids to be released. We found that intracellular stimulation of
putative histaminergic neurons in the L32 cluster of the abdominal
ganglion, which produces presynaptic inhibition in L10 neurons, also
elicited the release of 3H-12-HETE and 3H-PGE2. Thus, for the first time we
provide evidence that synaptic stimulation promotes turnover of arachidonic
acid in neurons. We suggest that metabolites of arachidonic acid are likely
to participate in some postsynaptic responses to histamine and may be
second messengers for presynaptic inhibition.
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