Intracellular Ca2+ modulates Cl- current evoked by acetylcholine in Lymnaea neurons.
The influence of voltage-gated Ca2+ current (ICa) on Cl current (ICl) initiated by nicotinic receptors (AChRs) in dialysed voltage-clamped Lymnaea neurons was studied. Depolarising steps applied before or during ACh application decreased ICl transiently and slowed down both the rising phase and decay of ICl. The effect of ICa depended on the interval between ICa and ICl; it was prevented by intracellular buffering with BAPTA or Ca2+ channel blocking with Ni2+. ISr had a similar action but the recovery was slower than after ICa; IBa was ineffective. The data suggest that inactivation of AChR channels is mediated by Ca2+ binding to a site in the AChR or the regulatory protein.
Institute of Cell Biophysics, Russian Academy of Sciences, Pushchino, Moscow Region. vulfius@receptor.iteb.serpukhov.su
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Vulfius
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Ryazansky
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Ilyasov
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001464:Barium / Q000502:physiology; D002118:Calcium / Q000378:metabolism* / Q000502:physiology; D018118:Chloride Channels / Q000502:physiology*; D005071:Evoked Potentials; D066298:In Vitro Techniques; D007424:Intracellular Fluid / Q000378:metabolism*; D015640:Ion Channel Gating; D008195:Lymnaea; D009474:Neurons / Q000187:drug effects* / Q000502:physiology; D018408:Patch-Clamp Techniques; D011978:Receptors, Nicotinic / Q000502:physiology; D013324:Strontium / Q000502:physiology
D018118:Chloride Channels; D011978:Receptors, Nicotinic; D001464:Barium; D000109:Acetylcholine; D002118:Calcium; D013324:Strontium