{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T10:31:39Z","timestamp":1772188299205,"version":"3.50.1"},"reference-count":47,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[1998,2,1]]},"abstract":"<jats:p>Li, Yu-Wen, Patrice G. Guyenet, and Douglas A. Bayliss. Voltage-dependent calcium currents in bulbospinal neurons of neonatal rat rostral ventrolateral medulla: modulation by \u03b1<jats:sub>2<\/jats:sub>-adrenergic receptors. J. Neurophysiol. 79: 583\u2013594, 1998. The properties and modulation by norepinephrine (NE) of voltage-dependent calcium currents were studied in bulbospinal neurons ( n = 116) of the rostral ventrolateral medulla (RVLM) using whole cell patch-clamp techniques in neonatal rat brain stem slices. RVLM bulbospinal neurons were identified visually by their location in slices and by the presence of flourescein isothiocyanate-tagged microbeads, which were injected into the spinal cord before the experiment; RVLM neurons were filled with Lucifer yellow during recordings, and the slice was processed for detection of tyrosine hydroxylase immunoreactivity (TH-IR). Thirty-four of 42 recovered cells (81%) were positive for TH-IR, indicating that most recorded cells were C1 neurons. Bulbospinal RVLM neurons expressed a prominent high-voltage\u2013activated (HVA) calcium current, which began to activate at \u221230 to \u221240 mV (from a holding potential of \u221260 or \u221270 mV), and peaked at \u223c0 mV (0.8 \u00b1 0.1 nA;mean \u00b1 SE). HVA current comprised predominantly \u03c9-conotoxin GVIA-sensitive, N-type and \u03c9-agatoxin IVA-sensitive, P\/Q-type components, with smaller dihydropyridine-sensitive, L-type, and residual current components. Most RVLM bulbospinal neurons ( n = 44\/52, including 12\/14 histologically identified C1 cells) also expressed low-voltage\u2013activated (LVA) calcium current. LVA current began to activate at \u223c\u221260 mV (from a holding potential of \u2212100 mV) and was nearly completely inactivated at \u221250 mV with a half-inactivation potential of \u221270 \u00b1 2 mV. The amplitude of LVA current at \u221250 mV was 78 \u00b1 24 pA with Ba<jats:sup>2+<\/jats:sup>and 156 \u00b1 38 pA with Ca<jats:sup>2+<\/jats:sup>as a charge carrier. NE inhibited HVA current in most bulbospinal RVLM neurons ( n = 70\/77) with an EC<jats:sub>50<\/jats:sub>of 1.2 \u03bcM; NE had no effect on LVA current. Calcium current inhibition by NE was mediated by \u03b1<jats:sub>2<\/jats:sub>-adrenergic receptors (\u03b1<jats:sub>2<\/jats:sub>-ARs) as the effect was mimicked by the selective \u03b1<jats:sub>2<\/jats:sub>-AR agonist, UK-14,304, and blocked by idazoxan, an \u03b1<jats:sub>2<\/jats:sub>-AR antagonist, but unaffected by prazosin and propranolol (\u03b1<jats:sub>1<\/jats:sub>- and \u03b2-AR antagonists, respectively). Most of the NE-sensitive calcium current was N- and P\/Q-type. NE-induced inhibition of calcium current evoked by action potential waveforms (APWs) was significantly larger than that evoked by depolarizing steps (34 \u00b1 2.5 vs. 23 \u00b1 2.7%; P &lt; 0.05). Although inhibition of calcium current was voltage dependent and partially relieved by strong depolarizations, when calcium currents were evoked with a 10-Hz train of APWs as a voltage command, the inhibitory effect of NE was maintained throughout the train. In conclusion, bulbospinal RVLM neurons, including C1 cells, express multiple types of calcium currents. Inhibition of HVA calcium current by NE may modulate input-output relationships and release of transmitters from C1 cells.<\/jats:p>","DOI":"10.1152\/jn.1998.79.2.583","type":"journal-article","created":{"date-parts":[[2017,12,25]],"date-time":"2017-12-25T07:07:11Z","timestamp":1514185631000},"page":"583-594","source":"Crossref","is-referenced-by-count":42,"title":["Voltage-Dependent Calcium Currents in Bulbospinal Neurons of Neonatal Rat Rostral Ventrolateral Medulla: Modulation by \u03b1<sub>2<\/sub>-Adrenergic Receptors"],"prefix":"10.1152","volume":"79","author":[{"given":"Yu-Wen","family":"Li","sequence":"first","affiliation":[{"name":"Department of Pharmacology, University of Virginia, Charlottesville, Virginia 22908"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Patrice G.","family":"Guyenet","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Virginia, Charlottesville, Virginia 22908"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Douglas A.","family":"Bayliss","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Virginia, Charlottesville, Virginia 22908"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"issue":"33","key":"B1","first-page":"R1065","volume":"265","author":"Allen A. 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