Sources of Ca2+ for different Ca(2+)-activated K+ conductances in neurones of the rat superior cervical ganglion.
1. The role of various Ca(2+)-activated K+ conductances were investigated using intracellular recording and single-electrode voltage clamp in neurones of superior cervical ganglia isolated in vitro from young adult rats. 2. Following replacement of Ca2+ with Co2+ (2 mM) or the addition of Cd2+ (100 microM), action potential amplitude and half-width either increased or decreased (in different cells), but both the after-hyperpolarization (AHP) and the outward tail current following a suprathreshold voltage step were markedly attenuated (by about 75%). 3. Addition of charybdotoxin (60 nM) or nifedipine (10 microM) increased action potential half-width (by about 25%) but had no significant effect on the AHP or tail current. 4. Addition of apamin (100 nM) or omega-conotoxin GVIA (100 nM) reduced the AHP and tail current (by about 60%) but did not significantly affect the action potential. A prolonged apamin-resistant component of the AHP present in 50% of neurones was blocked by ryanodine (20 microM). 5. Omega-Conotoxin MVIIC (150 nM) and omega agatoxin IVA (200 nM) had no significant effects on the action potential half-width or the AHP. 6. None of the Ca2+ channel blockers affected the prolonged ryanodine-sensitive component of the AHP and tail current. 7. We conclude that, in rat sympathetic neurones, Ca2+ entry via L-type channels selectively activates large conductance Ca(2+)-activated K+ channels (BK type) contributing to action potential repolarization, whereas Ca2+ entry via N-type channels selectively activates small conductance Ca(2+)-activated K+ channels (SK type) contributing to the AHP. Ca2+ entry via R-type Ca2+ channels prolongs the AHP by activating Ca2+ release from intracellular stores.
Prince of Wales Medical Research Institute, Randwick, NSW, Australia.
P J
PJ
Davies
D R
DR
Ireland
E M
EM
McLachlan
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D065168:Bradykinin Receptor Antagonists; D002118:Calcium / Q000378:metabolism* / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D003712:Dendrites / Q000187:drug effects / Q000502:physiology; D004594:Electrophysiology; D005260:Female; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000502:physiology; D008839:Microelectrodes; D009474:Neurons / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D018002:Receptors, Bradykinin / Q000378:metabolism; D017783:Superior Cervical Ganglion / Q000166:cytology / Q000378:metabolism*
D065168:Bradykinin Receptor Antagonists; D002121:Calcium Channel Blockers; D015221:Potassium Channels; D018002:Receptors, Bradykinin; D002118:Calcium