{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,6,29]],"date-time":"2025-06-29T06:10:01Z","timestamp":1751177401072,"version":"3.41.0"},"reference-count":42,"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>Adams, David J. and Carlo Trequattrini. Opioid receptor-mediated inhibition of \u03c9-conotoxin GVIA-sensitive calcium channel currents in rat intracardiac neurons. J. Neurophysiol. 79: 753\u2013762, 1998. Modulation of depolarization-activated ionic conductances by opioid receptor agonists was investigated in isolated parasympathetic neurons from neonatal rat intracardiac ganglia by using the whole cell perforated patch clamp technique. Met-enkephalin (10 \u03bcM) altered the action potential waveform, reducing the maximum amplitude and slowing the rate of rise and repolarization but the afterhyperpolarization was not appreciably altered. Under voltage clamp, 10 \u03bcM Met-enkephalin selectively and reversibly inhibited the peak amplitude of high-voltage\u2013activated Ca<jats:sup>2+<\/jats:sup>channel currents elicited at 0 mV by \u223c52% and increased three- to fourfold the time to peak. Met-enkephalin had no effect on the voltage dependence of steady-state inactivation but shifted the voltage dependence of activation to more positive membrane potentials whereby stronger depolarization was required to open Ca<jats:sup>2+<\/jats:sup>channels. Half-maximal inhibition of Ba<jats:sup>2+<\/jats:sup>current ( I<jats:sub>Ba<\/jats:sub>) amplitude was obtained with 270 nM Met-enkephalin or Leu-enkephalin. The opioid receptor subtype selective agonists, DAMGO and DADLE, but not DPDPE, inhibited I<jats:sub>Ba<\/jats:sub>and were antagonized by the opioid receptor antagonists, naloxone and naltrindole with IC<jats:sub>50<\/jats:sub>s of 84 nM and 1 \u03bcM, respectively. The \u03ba-opioid receptor agonists, bremazocine and dynorphin A, did not affect Ca<jats:sup>2+<\/jats:sup>channel current amplitude or kinetics. Taken together, these data suggest that enkephalin-induced inhibition of Ca<jats:sup>2+<\/jats:sup>channels in rat intracardiac neurons is mediated primarily by the \u03bc-opioid receptor type. Addition of Met-enkephalin after exposure to 300 nM \u03c9-conotoxin GVIA, which blocked \u223c75% of the total Ca<jats:sup>2+<\/jats:sup>channel current, failed to cause a further decrease of the residual current. Met-enkephalin inhibited the \u03c9-conotoxin GVIA-sensitive but not the \u03c9-conotoxin-insensitive I<jats:sub>Ba<\/jats:sub>in rat intracardiac neurons. Dialysis of the cell with a GTP-free intracellular solution or preincubation of the neurons in Pertussis toxin (PTX) abolished the attenuation of I<jats:sub>Ba<\/jats:sub>by Met-enkephalin, suggesting the involvement of a PTX-sensitive Gprotein in the signal transduction pathway. The activation of \u03bc-opioid receptors and subsequent inhibition of N-type Ca<jats:sup>2+<\/jats:sup>channels in the soma and terminals of postganglionic intracardiac neurons is likely to inhibit the release of ACh and thereby regulate vagal transmission to the mammalian heart.<\/jats:p>","DOI":"10.1152\/jn.1998.79.2.753","type":"journal-article","created":{"date-parts":[[2017,12,25]],"date-time":"2017-12-25T07:07:11Z","timestamp":1514185631000},"page":"753-762","source":"Crossref","is-referenced-by-count":22,"title":["Opioid Receptor-Mediated Inhibition of \u03c9-Conotoxin GVIA-Sensitive Calcium Channel Currents in Rat Intracardiac Neurons"],"prefix":"10.1152","volume":"79","author":[{"given":"David J.","family":"Adams","sequence":"first","affiliation":[{"name":"Department of Molecular and Cellular Pharmacology, University of Miami School of Medicine, Miami, Florida 33101; and Department of Physiology and Pharmacology, University of Queensland, Brisbane, Queensland 4072, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carlo","family":"Trequattrini","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cellular Pharmacology, University of Miami School of Medicine, Miami, Florida 33101; and Department of Physiology and Pharmacology, University of Queensland, Brisbane, Queensland 4072, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"B1","first-page":"1575","volume":"21","author":"Adams D. 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