INWARD CURRENTS UNDERLYING ACTION-POTENTIALS IN RAT ADRENAL CHROMAFFIN CELLS

Citation
B. Hollins et Sr. Ikeda, INWARD CURRENTS UNDERLYING ACTION-POTENTIALS IN RAT ADRENAL CHROMAFFIN CELLS, Journal of neurophysiology, 76(2), 1996, pp. 1195-1211
Citations number
37
Categorie Soggetti
Neurosciences,Physiology
Journal title
ISSN journal
00223077
Volume
76
Issue
2
Year of publication
1996
Pages
1195 - 1211
Database
ISI
SICI code
0022-3077(1996)76:2<1195:ICUAIR>2.0.ZU;2-W
Abstract
1. Current- and voltage-clamp studies were conducted on isolated rat a drenal chromaffin cells to identify the voltage-dependent ion channels mediating inward currents. 2. Mean resting membrane potential of the isolated cells was -62+/-3 (SE) mV. Evoked action potentials were both Na+ and Ca2+ based, and whole cell voltage-clamp studies in normal sa line revealed an inward-rectifier-type current. 3. Na+ channels were s tudied in isolation and showed a half-inactivation of -60+/-2 mV with a slope factor of -6 mV and a half-activation of -26.8+/-2 mV with a s lope factor of 6.5+/-0.7 mV. 4. Isolated Ca2+ currents, elicited in 10 mM external Ca2+, revealed a T-type current in a subset of cells. Ca2 + currents were sensitive to both N- and L-type channel antagonists, a nd blockade of the current by the L-type channel antagonist nimodipine and the N-type channel antagonist omega-conotoxin GVIA revealed a thi rd Ca2+ current component that was unaffected by the P-type channel an tagonist omega-agatoxin IVA. 5. Ca2+ currents were facilitated 5-20% b y a depolarizing prepulse, and facilitation was completely blocked by nimodipine. The effects of the dihydropyridine L-type channel agonist, (+)202-791 and depolarizing prepulses on the currents were additive. 6. The results of this study show that the properties of voltage-depen dent ion channels in rat chromaffin cells differ from those reported i n their counterparts in bovine chromaffin cells. Na+ channels differ i n activation and inactivation properties and Ca2+ channels differ in a ctivation, sensitivity to antagonists, and the magni tude of voltage-d ependent facilitation.