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Activation of Calcium Channel Currents in Rat Sensory Neurons by Large Depolarizations: Effect of Guanine Nucleotides and (‐)‐Baclofen
Author(s) -
Dolphin Annette C.,
Scott Roderick H.
Publication year - 1990
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1990.tb00386.x
Subject(s) - baclofen , biophysics , chemistry , calcium , depolarization , p type calcium channel , voltage dependent calcium channel , gtp' , gabab receptor , calcium channel , neuroscience , t type calcium channel , patch clamp , ion channel , electrophysiology , biochemistry , biology , antagonist , receptor , agonist , enzyme , organic chemistry
Calcium channel currents have been recorded from cultured rat sensory neurons at clamp potentials of between ‐30 and +120 mV. At large depolarizing potentials between +50 and +120 mV, the current was outward. This outward current was shown to be largely due to ions passing through calcium channels, because it was substantially although generally incompletely blocked by Cd 2+ (1 mM) and ω‐conotoxin (1 μM). Internal GTP‐γ‐S (100 μM) and to a lesser extent GTP (1 mM) reduced the amplitude and slowed the activation of the outward, as well as the inward calcium channel current. Baclofen (100 μM) reversibly inhibited both the inward and outward currents. These results suggest that the effect of baclofen and G protein activation on calcium channel currents is not due to a shift in the voltage‐dependence of channel availability.