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Journal of Neuroscience, Vol 15, 3679-3687, Copyright © 1995 by Society for Neuroscience
Arachidonic acid as a possible negative feedback inhibitor of nicotinic acetylcholine receptors on neurons
S Vijayaraghavan, B Huang, EM Blumenthal and DK Berg
Department of Biology, University of California at San Diego, La Jolla 92093-0357, USA.
Neuronal acetylcholine receptors, being highly permeable to calcium, are
likely to regulate calcium-dependent events in neurons. Arachidonic acid is
a membrane-permeant second messenger that can be released from membrane
phospholipids by phospholipases in a calcium-dependent manner. We show here
that activation of neuronal acetylcholine receptors triggers release of
3H-arachidonic acid in a calcium-dependent manner from neurons preloaded
with the fatty acid. Moreover, low concentrations of arachidonic acid
reversibly inhibit the receptors and act most efficiently on receptors
likely to have the highest permeability to calcium, namely receptors
containing alpha 7 subunits. Low concentrations of arachidonic acid also
reversibly inhibit alpha 7- containing receptors expressed in Xenopus
oocytes following injection of alpha 7 cRNA. The oocyte results indicate
following injection of alpha 7 cRNA. The oocyte results indicate that the
inhibition is a feature of the receptors rather than a consequence of
neuron-specific machinery. The inhibition is not mediated by specific
metabolites of arachidonic acid because the effects can be mimicked by
other fatty acids; their effectiveness correlates with their content of
double bonds. In contrast to arachidonic effects on calcium currents,
inhibition of neuronal nicotinic receptors by the fatty acid cannot be
prevented by blocking production of free radicals or by inhibiting protein
kinase C. An alternative mechanism is that arachidonic acid binds directly
to the receptors or perturbs the local environment in such a manner as to
constrain receptor function.(ABSTRACT TRUNCATED AT 250 WORDS)
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