Abstract
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 language | English (US) |
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Pages (from-to) | 1341-1350 |
Number of pages | 10 |
Journal | British journal of pharmacology |
Volume | 118 |
Issue number | 6 |
DOIs | |
State | Published - 1996 |
Keywords
- Autonomic nervous system
- Brainstem
- G-protein
- GABA(B) receptor
- Pertussis toxin
- Somatostatin
- μ-opioid receptor
ASJC Scopus subject areas
- Pharmacology