Ionic mechanisms mediating the acetylcholine-elicited contraction in Aplysia buccal muscle.
Ion channel mechanisms mediating acetylcholine (ACh)-elicited contractions in Aplysia buccal muscles were investigated using conventional force and membrane potential recording techniques and whole-cell voltage clamping of dissociated buccal muscle fibers. Previous work on buccal muscles of Aplysia showed that acetylcholine (ACh) depolarizes muscle fibers to, at most, -30 mV and that contraction is dependent upon extracellular calcium. In intact muscle, removal of either calcium or sodium from the extracellular medium reduced ACh-elicited depolarization. Absence of each ion reduced the depolarization approximately 50% at low [ACh], but at high [ACh], absence of sodium had a greater effect, while absence of calcium had a proportionally smaller effect on depolarization. Nifedipine (3 microM) reduced contraction by 50% with little accompanying change in depolarization. In whole cell voltage-clamping of isolated muscle fibers, ACh elicited an inward current at resting potential. The reversal potential for ACh-elicited current was -24 +/- 6 mV. The current-voltage curve was rectified, with a bend in the inward direction near -35 mV. In zero calcium medium, ACh-elicited current averaged 54% of control, and in zero sodium medium, 42% of control. Nifedipine reduced ACh-elicited current by less than 20%. Amiloride, an inhibitor of Aplysia buccal muscle contraction, reduced ACh-elicited current by 30-70%. A model based on the above results is that ACh depolarizes muscle fibers by opening channels with a reversal potential of about -30 mV that are permeable to calcium, sodium, and at least one other ion. Depolarization activates voltage-dependent calcium channels, enabling activator calcium to enter the fibers through both ACh-operated and voltage-dependent channels.
Liu
L X
LX
Department of Physiology, Wayne State University, Detroit, MI 48201.
Ram
J L
JL
D000109:Acetylcholine / Q000494:pharmacology*; D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D001048:Aplysia / Q000502:physiology*; D004594:Electrophysiology; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism*; D008564:Membrane Potentials / Q000187:drug effects; D009119:Muscle Contraction / Q000187:drug effects; D009132:Muscles / Q000187:drug effects* / Q000378:metabolism; D009467:Neuromuscular Depolarizing Agents / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology
D007473:Ion Channels; D009467:Neuromuscular Depolarizing Agents; D000584:Amiloride; D009543:Nifedipine; D000109:Acetylcholine