Effects of ATP and GTP on voltage-gated K+ currents in glandular and muscular sympathetic neurons.
This study assesses the effects of ATP and GTP on the kinetic properties of voltage-gated K+ currents in anatomically identified postganglionic sympathetic neurons innervating the submandibular gland and the masseter muscle in rats. Three types of K+ currents were isolated: the I(Af) steady-state inactivating at more hyperpolarized potentials, I(As) steady-state inactivating at less hyperpolarized potentials than I(Af) and the I(K) current independent of membrane potential. The kinetic properties of these currents were tested in neurons with ATP (4 mM) and GTP (0.5 mM) or without ATP and GTP in the intracellular solution. In glandular and muscular neurons in the absence of ATP and GTP in the intracellular solution, the current density of I(Af) was significantly larger (142 pA/pF and 166 pA/pF, respectively) comparing to cells with ATP and GTP (96 pA/pF and 100 pA/pF, respectively). The I(As) was larger only in glandular neurons (52 pA/pF vs. 37 pA/pF).Conversely, I(K) current density was smaller in glandular and muscular neurons without ATP and GTP (17 pA/pF and 31 pA/pF, respectively) comparing to cells with ATP and GTP (57 pA/pF and 58 pA/pF, respectively). In glandular (15.5 nA/ms vs. 6.9 nA/ms) and muscular (10.9 nA/ms vs. 7.5 nA/ms) neurons, the I(Af) activated faster in the absence of ATP and GTP. Half inactivation voltage of I(Af) in glandular (-110.0 mV vs. -119.7 mV) and muscular (-108.4 vs. -117.3 mV) neurons was shifted towards depolarization in the absence of ATP and GTP. We suggest that the kinetic properties of K+ currents in glandular and muscular sympathetic neurons change markedly in the absence of ATP and GTP in the cytoplasm. Effectiveness of steady-state inactivated currents (I(Af) and I(AS)) increased, while effectiveness of steady-state noninactivated currents decreased in the absence of ATP and GTP. The effects were more pronounced in glandular than in muscular neurons.
Szulczyk
Bartłomiej
B
The Faculty of Medicine, Department of Experimental and Clinical Physiology, The Medical University of Warsaw, Krakowskie Przedmieście 26/28, Warsaw 00-927, Poland. szulczyk@amwaw.edu.pl
Rola
Rafał
R
Witkowski
Grzegorz
G
Szulczyk
Paweł
P
D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D002469:Cell Separation; D004594:Electrophysiology; D005434:Flow Cytometry; D006160:Guanosine Triphosphate / Q000494:pharmacology*; D015640:Ion Channel Gating / Q000502:physiology*; D007700:Kinetics; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D018482:Muscle, Skeletal / Q000187:drug effects / Q000294:innervation* / Q000378:metabolism*; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism*; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D015222:Sodium Channels / Q000187:drug effects / Q000378:metabolism; D013363:Submandibular Gland / Q000187:drug effects / Q000294:innervation* / Q000378:metabolism*; D013564:Sympathetic Nervous System / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism*
D026902:Potassium Channel Blockers; D015221:Potassium Channels; D015222:Sodium Channels; D006160:Guanosine Triphosphate; D000255:Adenosine Triphosphate