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Journal of Neuroscience, Vol 14, 889-896, Copyright © 1994 by Society for Neuroscience
Neuronal acetylcholine receptors that bind alpha-bungarotoxin mediate neurite retraction in a calcium-dependent manner
PC Pugh and DK Berg
Department of Biology, University of California at San Diego, La Jolla 92093-0357.
Neuronal membrane components that bind alpha-bungarotoxin with high
affinity have only recently been shown unambiguously to function as
nicotinic receptors. Activation of the receptors increases intracellular
levels of free calcium in neurons. In the chick ciliary ganglion, where the
receptors have been studied in some detail, they have been shown to have a
predominantly nonsynaptic location on neurons and may be concentrated on
pseudodendrites emerging from the somata. This has raised questions about
the physiological significance of the receptors for the neurons. Here we
show that activation of the receptors on isolated ciliary ganglion neurons
in cell culture produces neurite retraction. Focal application of either
nicotine or ACh at low concentrations induces the retraction, and
alpha-bungarotoxin blocks the effect. The retraction requires external
calcium and is confined to the individual neurite stimulated with agonist.
Brief exposure to elevated concentrations of K+ also induces neurite
retraction, and both the K(+)-induced and the nicotine-induced retractions
can be prevented by the calcium channel blocker omega-conotoxin. The
results suggest that activation of the alpha-bungarotoxin-binding nicotinic
receptors on neurites triggers activation of voltage-gated calcium channels
presumably by depolarizing the membrane, and that together they permit
sufficient calcium to enter the neurite to prevent further outgrowth and
induce retraction.
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