Mechanism of inhibition of calcium channels in rat nucleus tractus solitarius by neurotransmitters

Hyewhon Rhim, Peter T. Toth, Richard J. Miller*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

35 Scopus citations


1 High-threshold Ca2+ channel currents were measured every 15 s following a 200 ms voltage step from -80 mV to 0 mV in order to study the coupling mechanism between neurotransmitter receptors and Ca2+ channels in neurones acutely isolated from the nucleus tractus solitarius (NTS) of the rat. 2 Application of 30 μM baclofen (GABA(B) receptor agonist) caused 38.9 ± 1.2% inhibition of the peak inward Ba2+ current (I(Ba2+)) in most NTS cells tested (n = 85 of 88). Somatostatin, 300 nM, also reduced I(Ba2+) by 31.3 ± 1.6% in 53 cells of 82 tested. 3 Activation of μ-opioid-, GABA(B)- or somatostatin-receptors inhibited both N- and P/Q-type Ca2+ channels. 4 The inhibition of Ca2+ currents by DAMGO (μ-opioid receptor agonist), baclofen and somatostatin was reduced by treatment with pertussis toxin and partially relieved by application of a 50 ms conditioning prepulse to +80 mV. This suggests that a pertussis toxin-sensitive G-protein was involved in the neurotransmitter-mediated action in the observed inhibition of Ca2+ currents. 5 Intracellular loading with an antiserum raised against the amino terminus of G(0α) (GC/2) markedly attenuated the somatostatin-induced inhibition, but did not block the DAMGO- and baclofen-induced inhibition. 6 These findings suggest at least two different pertussis toxin-sensitive G-protein-mediated pathways are involved in receptor-induced inhibition of Ca2+ currents in the NTS.

Original languageEnglish (US)
Pages (from-to)1341-1350
Number of pages10
JournalBritish journal of pharmacology
Issue number6
StatePublished - 1996


  • Autonomic nervous system
  • Brainstem
  • G-protein
  • GABA(B) receptor
  • Pertussis toxin
  • Somatostatin
  • μ-opioid receptor

ASJC Scopus subject areas

  • Pharmacology


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