MUSCARINIC-RECEPTOR ACTIVATION STIMULATES OSCILLATIONS IN K- CURRENTSWHICH ARE ACUTELY DEPENDENT ON EXTRACELLULAR CA2+ IN AVIAN SALT-GLANDCELLS( AND CL)
Sc. Martin et Tj. Shuttleworth, MUSCARINIC-RECEPTOR ACTIVATION STIMULATES OSCILLATIONS IN K- CURRENTSWHICH ARE ACUTELY DEPENDENT ON EXTRACELLULAR CA2+ IN AVIAN SALT-GLANDCELLS( AND CL), Pflugers Archiv, 426(3-4), 1994, pp. 231-238
By utilizing the perforated-patch variant of the whole-cell patch-clam
p recording technique, in order to maintain the integrity of the norma
l cellular buffering systems, we demonstrate that carbachol (CCh) stim
ulates simultaneous oscillations in a Ca2+ and voltage-activated K+ cu
rrent and a linear Ca2+-activated Cl- current in an exocrine avian sal
t gland cell preparation. Similar conductance changes, although sustai
ned rather than oscillatory, are stimulated by the Ca2+ ionophore A231
87. The outward K+ current can be inhibited by tetraethylammonium chlo
ride (TEA) whereas the Cl- current is inhibited by the Cl- channel blo
ckers 5-nitro-2-(3-phenylpropylamino) (NPPB) and N-phenylanthranilic a
cid (DPC). The oscillations in current stimulated by CCh are acutely d
ependent on extracellular Ca2+ and are not affected by the application
of low doses of caffeine. In addition, the application of caffeine at
all doses fails to mimic the current transients stimulated by CCh. As
both caffeine and A23187 are unable to stimulate oscillations under t
he perforated-patch conditions we suggest that in avian salt gland cel
ls the primary oscillatory mechanism probably involves a one-pool mech
anism of Ca2+ release which is intimately related to the activation of
a Ca2+ influx pathway.