Title

Calcium permeability and modulation of nicotinic acetylcholine receptor-channels in rat parasympathetic neurons

RIS ID

106179

Publication Details

Adams, D. J. & Nutter, T. J. (1992). Calcium permeability and modulation of nicotinic acetylcholine receptor-channels in rat parasympathetic neurons. Journal of Physiology (Paris), 86 (1-3), 67-76.

Abstract

Neuronal nicotinic acetylcholine (ACh)-activated currents in rat parasympathetic ganglion cells were examined using whole-cell and single-channel patch clamp recording techniques. The whole-cell current-voltage (I-V) relationship exhibited strong inward rectification and a reversal (zero current) potential of -3.9 mV in nearly symmetrical Na+ solutions (external 140 mM Na+/internal 160 mM Na+). Isosmotic replacement of extracellular Na+ with either Ca2+ or Mg2+ yielded the permeability (PX/PNa) sequence Mg2+ (1.1) > Na+ (1.0) > Ca2+ (0.65). Whole-cell ACh-induced current amplitude decreased as [Ca2+]0 was raised from 2.5 mM to 20 mM, and remained constant at higher [Ca2+]0. Unitary ACh-activated currents recorded in excised outside-out patches had conductances ranging from 15-35 pS with at least three distinct conductance levels (33 pS, 26 pS, 19 pS) observed in most patches. The neuronal nicotinic ACh receptor-channel had a slope conductance of 30 pS in Na+ external solution, which decreased to 20 pS in isotonic Ca2+ and was unchanged by isosmotic replacement of Na+ with Mg2+. ACh-activated single channel currents had an apparent mean open time (τ0) of 1.15 ± 0.16 ms and a mean burst length (τb) of 6.83 ± 1.76 ms at -60 mV in Na+ external solution. Ca2+-free external solutions, or raising [Ca2+]0 to 50-100 mM decreased both the τ0 and τb of the nAChR channel. Varying [Ca2+]0 produced a marked decrease in NP0, while substitution of Mg2+ for Na+ increased NP0. These data suggest that activation of the neuronal nAChR channel permits a substantial Ca2+ influx which may modulate Ca2+-dependent ion channels and second messenger pathways to affect neuronal excitability in parasympathetic ganglia.

Please refer to publisher version or contact your library.

Share

COinS
 

Link to publisher version (DOI)

http://dx.doi.org/10.1016/S0928-4257(05)80009-9