K+-evoked taurine efflux from cerebellar astrocytes: on the roles of Ca2+ and Na+.
The ionic requirements for K+-evoked efflux of endogenous taurine from primary cerebellar astrocyte cultures were studied. The Ca2+ ionophore A23187 evoked taurine efflux in a dose-dependent fashion with a time-course identical to that of K+-induced efflux. The Ca2+-channel antagonist nifedipine had no effect upon efflux induced by 10 or 50 mM K+. In addition, verapamil did not antagonize 50 mM K+-evoked efflux except at high, non-pharmacological concentrations (greater than 100 microM), and preincubation with 2 microM omega-conotoxin had no effect on 50 mM K+-evoked efflux. Similarly, preincubation with 1 mM ouabain had no effect on the amount of taurine released by K+ stimulation, but did accelerate the onset of efflux by 2-4 min. Although 2 microM tetrodotoxin had no effect on K+-evoked release, replacing Na+ with choline abolished the taurine efflux seen in response to K+ stimulation. Together, these findings suggest that neuronal N- and L-type Ca2+- and voltage-dependent Na+-channels are not involved in the influx of Ca2+ which appears to be necessary for K+-evoked taurine efflux, and that in addition to Ca2+, extracellular Na+ is also required.
Philibert
R A
RA
Department of Pharmacology, College of Medicine, University of Iowa, Iowa City, IA 52242.
Rogers
K L
KL
Dutton
G R
GR
D000818:Animals; D001253:Astrocytes / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000502:physiology*; D002478:Cells, Cultured; D002531:Cerebellum / Q000166:cytology*; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology; D011188:Potassium / Q000494:pharmacology*; D051381:Rats; D012964:Sodium / Q000502:physiology*; D013654:Taurine / Q000378:metabolism*
D007473:Ion Channels; D013654:Taurine; D000001:Calcimycin; D012964:Sodium; D011188:Potassium; D002118:Calcium