M. Amador et Ja. Dani, MECHANISM FOR MODULATION OF NICOTINIC ACETYLCHOLINE-RECEPTORS THAT CAN INFLUENCE SYNAPTIC TRANSMISSION, The Journal of neuroscience, 15(6), 1995, pp. 4525-4532
Only recently has it been appreciated that neuronal nicotinic ACh rece
ptors (NnAChRs) are highly permeable to Ca2+ and are modulated by Ca2 in a dose-dependent manner, These findings suggest that Ca2+ could ha
ve roles in cholinergic synaptic plasticity, We report a possible mech
anism for Ca2+-initiated synaptic plasticity that differs from the int
racellular Ca2+ cascade associated with plasticity of glutamatergic sy
napses, Rapid changes in external Ca2+ modulate cholinergic spontaneou
s synaptic currents in superior cervical ganglionic sympathetic neuron
s, Inhibition of cholinergic currents by chlorisondamine, which blocks
only open channels and becomes trapped in the pore, showed that the m
odulation is not by a mechanism that activates a previously unresponsi
ve population of NnAChRs, Rather, single-channel recordings with gangl
ionic NnAChRs from chromaffin cells indicated that Ca2+ directly alter
s the probability of the channels being open, We hypothesize from the
results that activity-dependent decreases in external Ca2+, which occu
r throughout the nervous system, could directly underlie a rapid negat
ive-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 recep
tors until the external Ca2+ concentration recovers.