Does intracellular release of Ca2+ participate in the afterhyperpolarization of a sympathetic neurone?
The afterhyperpolarization (AHP) of an action potential in the bullfrog sympathetic ganglion cell was highly sensitive to anions (a factor affecting Ca2+ release) filled in a recording electrode; it was slower for citrate ion than for Cl-. The AHP recorded with a 'KCl-electrode' was suppressed drastically by D-600 (Ca2+-antagonist) and prolonged significantly by caffeine (promoting Ca2+ release), while the AHP recorded with a 'K3-citrate-electrode' was affected only slightly by these agents. Thus, these results suggest that Ca2+ entry during an action potential is the main origin of Ca2+ for the AHP recorded with a 'KCl-electrode', and favour the idea that the intracellular release of Ca2+ by an action potential as well as the Ca2+ influx participates in the mechanism of the AHP recorded with a 'K3-citrate-electrode'.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D004594:Electrophysiology; D005711:Gallopamil / Q000494:pharmacology; D005728:Ganglia, Sympathetic / Q000166:cytology*; D007425:Intracellular Membranes / Q000378:metabolism*; D009474:Neurons / Q000502:physiology*; D011892:Rana catesbeiana
D005711:Gallopamil; D002110:Caffeine; D002118:Calcium