Calcium-dependent potassium conductance in neurons of rabbit vesical pelvic ganglia.
Intracellular recordings were made from neurons of vesical pelvic (parasympathetic) ganglia (VPG) isolated from the rabbit urinary bladder. Spontaneous hyperpolarizations (SH), occurring at intervals of 30 s to 5 min, could be recorded from 53% of VPG neurons in Krebs solution. The action potential was associated with inward sodium and calcium currents and was followed by fast and slow afterhyperpolarizations (AHPs). The action potential also evoked an additional hyperpolarization which was identical to the SH. The SH and the AHPs were associated with a decrease in the input resistance and reversed their polarity close to the potassium equilibrium potential. Intracellular cesium ions blocked the AHPs and the SH. Superfusing the preparation with a calcium-free solution produced a depolarization associated with an increased input resistance. The outward rectification activated at the resting membrane potential was depressed in the calcium-free solution. The removal of extracellular calcium ions also depressed both the SH and the spike AHPs. Bath-application of caffeine (1-3 mM) increased the frequency of the appearance of the SH. Injection of EGTA into VPG neurons caused a depolarization due to a blockade of the outward rectification. EGTA also depressed the slow AHP and the SH. These results suggest that the neuronal membrane of the rabbit VPG is endowed with a calcium-dependent potassium conductance (gKCa). Apamin (0.3-5 nM) and (+)-tubocurarine (30-300 microM) blocked the slow AHP and the SH without affecting the fast AHP and the resting membrane potential. Tetraethylammonium (TEA, 0.3-5 mM) suppressed the fast AHP and the SH without affecting the outward rectification. TEA augmented the slow AHP. Barium ions (0.1-1 mM) depressed the AHPs, the SH and the outward rectification. These pharmacological properties imply that at least 3 kinds of gKCa systems underlie the generation of the outward rectification, the spike AHPs and the SH.
Nishimura
T
T
Department of Physiology, Kurume University School of Medicine, Japan.
Tokimasa
T
T
Akasu
T
T
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001030:Apamin / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology*; D004533:Egtazic Acid / Q000494:pharmacology; D004553:Electric Conductivity; D005726:Ganglia, Parasympathetic / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D010388:Pelvis / Q000502:physiology*; D011188:Potassium / Q000494:pharmacology*; D011817:Rabbits; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D014403:Tubocurarine / Q000494:pharmacology
D013757:Tetraethylammonium Compounds; D001030:Apamin; D004533:Egtazic Acid; D019789:Tetraethylammonium; D011188:Potassium; D002118:Calcium; D014403:Tubocurarine