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Journal of Neuroscience, Vol 15, 4525-4532, Copyright © 1995 by Society for Neuroscience
Mechanism for modulation of nicotinic acetylcholine receptors that can influence synaptic transmission
M Amador and JA Dani
Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030-3498, USA.
Only recently has it been appreciated that neuronal nicotinic ACh receptors
(NnAChRs) are highly permeable to Ca2+ and are modulated by Ca2+ in a
dose-dependent manner. These findings suggest that Ca2+ could have roles in
cholinergic synaptic plasticity. We report a possible mechanism for
Ca(2+)-initiated synaptic plasticity that differs from the intracellular
Ca2+ cascade associated with plasticity of glutamatergic synapses. Rapid
changes in external Ca2+ modulate cholinergic spontaneous synaptic currents
in superior cervical ganglionic sympathetic neurons. Inhibition of
cholinergic currents by chlorisondamine, which blocks only open channels
and becomes trapped in the pore, showed that the modulation is not by a
mechanism that activates a previously unresponsive population of NnAChRs.
Rather, single-channel recordings with ganglionic NnAChRs from chromaffin
cells indicated that Ca2+ directly alters the probability of the channels
being open. We hypothesize from the results that activity-dependent
decreases in external Ca2+, which occur throughout the nervous system,
could directly underlie a rapid negative-feedback mechanism that decreases
the responsiveness of NnAChRs at synapses. When external Ca2+ is decreased,
presynaptic Ca2+ currents and transmitter release also are diminished.
Thus, several mechanisms could combine to potently and rapidly depress
synaptic nicotinic receptors until the external Ca2+ concentration
recovers.
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