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• W2017483076 abstract "Whole-cell patch-clamp recordings were obtained from nodose ganglion neurons acutely dissociated from 10–30-day-old rats to characterize the Ca2+ channel types that are modulated by GABAB and μ-opioid receptors. Five components of high-threshold current were distinguished on the basis of their sensitivity to blockade by ω-conotoxin GVIA, nifedipine, ω-agatoxin IVA and ω-conotoxin MVIIC. Administration of the μ-opioid agonist H-Tyr-D-Ala-Gly-Phe(N-Me)-Gly-ol (0.3–1 mM) or the GABAB agonist baclofen in saturating concentrations suppressed high-threshold Ca2+ currents by 49.9±2.4% n=69) and 18.7±2.1% n=35), respectively. The inhibition by H-Tyr-D-Ala-Gly-Phe(N-Me)-Gly-ol exceeded that by baclofen in virtually all neurons that responded to both agonists (67%), and occlusion experiments revealed that responses to μ-opioid and GABAB receptor activation were not linearly additive. In addition, administration of staurosporine, a non-selective inhibitor of protein kinase A and C, did not affect the inhibitory responses to either agonist or prevent the occlusion of baclofen-induced current inhibition by H-Tyr-D-Ala-Gly-Phe(N-Me)-Gly-ol. Blockade of N-type channels by ω-conotoxin GVIA eliminated current suppression by baclofen in all cells tested n=11). μ-Opioid-induced inhibition in current was abolished by ω-conotoxin GVIA in 12 of 30 neurons tested, but was only partially reduced in the remaining 18 neurons. In the latter cells administration of ω-agatoxin IVA reduced, but did not eliminate the μ-opioid sensitive current component that persisted after blockade of N-type channels. This residual component of μ-opioid-sensitive current was blocked completely by ω-conotoxin MVIIC in nine neurons, whereas responses to H-Tyr-D-Ala-Gly-Phe(N-Me)-Gly-ol were still recorded in the remaining cells after administration of these Ca2+ channel toxins and nifedipine. Dihydropyridine-sensitive (L-type) current was not affected by activation of μ-opioid or GABAB receptors in any of the neurons. These data indicate that in nodose ganglion neurons μ-opioid receptors are negatively coupled to N-, P- and Q-type channels as well as to a fourth, unidentified toxin-resistant Ca2+ channel. In contrast, GABAB receptors are coupled only to N-type channels. Furthermore, the results do not support a role for either protein kinase C or A in the modulatory pathway(s) coupling μ-opioid and GABAB receptors to Ca2+ channels, but rather lend credence to the notion that the signalling mechanisms utilized by these two receptors might simply compete for inhibitory control of a common pool of N-type channels." @default.
• W2017483076 created "2016-06-24" @default.
• W2017483076 creator A5018876370 @default.
• W2017483076 creator A5055757409 @default.
• W2017483076 date "1998-04-01" @default.
• W2017483076 modified "2023-09-25" @default.
• W2017483076 title "μ-Opioid and GABAB receptors modulate different types of Ca2+ currents in rat nodose ganglion neurons" @default.
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• W2017483076 doi "https://doi.org/10.1016/s0306-4522(97)00674-x" @default.
• W2017483076 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9639286" @default.
• W2017483076 hasPublicationYear "1998" @default.
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