INHIBITORY EFFECTS OF ARACHIDONIC ACID ON NICOTINIC TRANSMISSION IN
BULLFROG SYMPATHETIC NEURONS.
SHOICHI MINOTA and SADAHIRO WATANABE.
Division of Basic Medical Science, Kobe City College of Nursing, Nishi-ku,
Kobe 651-21, Japan
APStracts 4:130N, 1997.
ABSTRACT
Arachidonic acid (AA, 0.2-40 uM) reversibly reduced the ampli-
tude of the fast excitatory post-synaptic potentials (fast EPSPs)
and the underlying currents (fast EPSCs) of bullfrog sympathetic
neurons evoked by preganglionic nerve stimulation in a Ca2+-
deficient solution. AA reduced the acetylcholine(ACh)-induced
nicotinic currents (nIACh) evoked by brief applications of ACh to
the ganglion cells in a dose-related manner. AA reduced the
maximum amplitude of nIACh estimated from the dose-response
relationship without causing an appreciable change in the appar-
ent dissociation constant. Indomethacin (2 uM) and nordihydro-
guaiaretic acid (NDGA,20 uM), blockers of cyclooxygenase and
lipoxygenase pathways, respectively, had no effect on the inhibi-
tion of fast EPSC by AA. AA did not obviously affect the pregan-
glionic nerve terminal spike configuration, synaptic delay,
facilitation, quantal content of transmitter release and the
presynaptic long-term potentiation elicited by the repetitive
stimulation applied to the preganglionic nerve fibers.
These results suggest that AA acts on an allosteric site of
the nicotinic receptor-channel complex either directly or indi-
rectly and in turn inhibits ion permeation through these channels
without affecting the release of ACh from preganglionic nerve
terminals.
Received 12 March 1997; accepted in final form 7 July 1997.
APS Manuscript Number J210-7.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 24 July 1997