{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T05:17:47Z","timestamp":1773292667722,"version":"3.50.1"},"reference-count":42,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[2001,7,1]]},"abstract":"<jats:p>The effect of a nitric oxide (NO) donor on high-voltage-activated Ca<jats:sup>2+<\/jats:sup>channel currents ( I<jats:sub>Ca<\/jats:sub>) was examined using the whole cell patch-clamp technique in L<jats:sub>6<\/jats:sub>\u2013S<jats:sub>1<\/jats:sub>dorsal root ganglion (DRG) neurons innervating the urinary bladder. The neurons were labeled by axonal transport of a fluorescent dye, Fast Blue, injected into the bladder wall. Approximately 70% of bladder afferent neurons exhibited tetrodotoxin (TTX)-resistant action potentials (APs), and 93% of these neurons were sensitive to capsaicin, while the remaining neurons had TTX-sensitive spikes and were insensitive to capsaicin. The peak current density of nimodipine-sensitive L-type Ca<jats:sup>2+<\/jats:sup>channels activated by depolarizing pulses (0 mV) from a holding potential of \u221260 mV was greater in bladder afferent neurons with TTX-resistant APs (39.2 pA\/pF) than in bladder afferent neurons with TTX-sensitive APs (28.9 pA\/pF), while the current density of \u03c9-conotoxin GVIA-sensitive N-type Ca<jats:sup>2+<\/jats:sup>channels was similar (43\u201345 pA\/pF) in both types of neurons. In both types of neurons, the NO donor, S-nitroso- N-acetylpenicillamine (SNAP) (500 \u03bcM), reversibly reduced (23.4\u201326.6%) the amplitude of I<jats:sub>Ca<\/jats:sub>elicited by depolarizing pulses to 0 mV from a holding potential of \u221260 mV. SNAP-induced inhibition of I<jats:sub>Ca<\/jats:sub>was reduced by 90% in the presence of \u03c9-conotoxin GVIA but was unaffected in the presence of nimodipine, indicating that NO-induced inhibition of I<jats:sub>Ca<\/jats:sub>is mainly confined to N-type Ca<jats:sup>2+<\/jats:sup>channels. Exposure of the neurons for 30 min to 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 10 \u03bcM), an inhibitor of NO-stimulated guanylyl cyclase, prevented the SNAP-induced reduction in I<jats:sub>Ca<\/jats:sub>. Extracellular application of 8-bromo-cGMP (1 mM) mimicked the effects of NO donors by reducing the peak amplitude of I<jats:sub>Ca<\/jats:sub>(28.6% of reduction). Action potential configuration and firing frequency during depolarizing current pulses were not altered by the application of SNAP (500 \u03bcM) in bladder afferent neurons with TTX-resistant and -sensitive APs. These results indicate that NO acting via a cGMP signaling pathway can modulate N-type Ca<jats:sup>2+<\/jats:sup>channels in DRG neurons innervating the urinary bladder.<\/jats:p>","DOI":"10.1152\/jn.2001.86.1.304","type":"journal-article","created":{"date-parts":[[2017,12,21]],"date-time":"2017-12-21T10:54:56Z","timestamp":1513853696000},"page":"304-311","source":"Crossref","is-referenced-by-count":102,"title":["Nitric Oxide Modulates Ca<sup>2+<\/sup>Channels in Dorsal Root Ganglion Neurons Innervating Rat Urinary Bladder"],"prefix":"10.1152","volume":"86","author":[{"given":"Naoki","family":"Yoshimura","sequence":"first","affiliation":[{"name":"Department of Pharmacology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Satoshi","family":"Seki","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 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