Modulation of M-current by intracellular Ca2+.
IM is a voltage- and time-dependent K+ current that is suppressed by muscarinic receptor activation. IM augmentation following agonist washout was blocked by heavily buffering [Ca2+]i using BAPTA. Although IM is not primarily Ca2+ dependent, small increases in [Ca2+]i by photolysis of the "caged" Ca2+ chelator nitr-5 or by evoking action potentials augmented, while larger increases inhibited, IM. Raising [Ca2+]i for prolonged periods, by nitr-5 photolysis, reduced its sensitivity to agonist, leaving a poorly reversible response. These results suggest that IM can be regulated by physiologically relevant changes in [Ca2+]i, placing IM in a unique position to modulate cell excitability.
Marrion
N V
NV
Howard Hughes Medical Institute, State University of New York, Stony Brook 11794.
Zucker
R S
RS
Marsh
S J
SJ
Adams
P R
PR
D000818:Animals; D002021:Buffers; D002118:Calcium / Q000502:physiology*; D002614:Chelating Agents; D004533:Egtazic Acid / Q000494:pharmacology / Q000031:analogs & derivatives; D005071:Evoked Potentials; D007425:Intracellular Membranes / Q000502:physiology*; D009474:Neurons / Q000502:physiology*; D010782:Photolysis; D011188:Potassium / Q000502:physiology*; D011892:Rana catesbeiana; D013564:Sympathetic Nervous System / Q000166:cytology / Q000502:physiology*
D002021:Buffers; D002614:Chelating Agents; C052455:nitr 5; D004533:Egtazic Acid; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid; D011188:Potassium; D002118:Calcium