Properties of Ca2+ currents in acutely dissociated neurons of the chick ciliary ganglion: inhibition by somatostatin-14 and somatostatin-28.
Whole-cell voltage-clamp recordings were made from acutely dissociated neurons obtained from the embryonic chick ciliary ganglion. Recording pipettes were filled with salines containing 120 mM CsCl or 120 mM tetraethylammonium-Cl. Application of depolarizing voltage commands evoked L-type Ca2+ currents and, at voltages positive to 0 mV, an unidentified cationic conductance. The unidentified cationic conductances made the Ca2+ currents appear to undergo voltage-dependent inactivation and made a large contribution to tail currents present during repolarizing voltage steps. Ca2+ Ca2+ currents showed little or no sign of inactivation and did not reverse at voltages up to +60 mV. Application of somatostatin-14 or somatostatin-28 produced a reversible inhibition of Ca2+ currents in virtually all cells, regardless of size. Somatostatin-28 (1-14) was inactive. The effects of somatostatin-14 and somatostatin-28 were attenuated by pretreatment with pertussis toxin, suggesting a role for G-proteins in mediating the response. Somatostatin-14 and somatostatin-28 had no effect on voltage-dependent K+ currents. The results suggest that somatostatin peptides modulate the motor output of the chick ciliary ganglion.
Dryer
S E
SE
Department of Biological Science, Florida State University, Tallahassee 32306-3050.
Dourado
M M
MM
Wisgirda
M E
ME
D015761:4-Aminopyridine / Q000494:pharmacology; D000109:Acetylcholine / Q000378:metabolism; D000200:Action Potentials / Q000187:drug effects*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology*; D002478:Cells, Cultured; D002642:Chick Embryo; D019204:GTP-Binding Proteins / Q000037:antagonists & inhibitors / Q000502:physiology; D005726:Ganglia, Parasympathetic / Q000166:cytology*; D015640:Ion Channel Gating / Q000187:drug effects*; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D009543:Nifedipine / Q000494:pharmacology; D037342:Pertussis Toxin; D011188:Potassium / Q000378:metabolism; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology; D013004:Somatostatin / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D053561:Somatostatin-28; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D010566:Virulence Factors, Bordetella / Q000494:pharmacology
D015220:Calcium Channels; D015221:Potassium Channels; D013757:Tetraethylammonium Compounds; D010566:Virulence Factors, Bordetella; D013779:Tetrodotoxin; D013004:Somatostatin; D019789:Tetraethylammonium; D053561:Somatostatin-28; D015761:4-Aminopyridine; D037342:Pertussis Toxin; D019204:GTP-Binding Proteins; D009543:Nifedipine; D000109:Acetylcholine; D011188:Potassium; D002118:Calcium