Abstract
High- and low-voltage activated calcium channel currents (HVA and LVA) were inhibited by acetylcholine (10–100 μM) and baclofen (10 μM) in adult rat sensory neurons. This modulatory effect was present on dihydropyridine (nifedipine 1 μM) and/or ω-conotoxin (3.2 μM, 2–5 h incubation) insensitive components and was insensitive to holding potentials ( V h −50 to −90 mV). GTP- γ- S (100 μM) prolonged calcium channel current activation in a time- and voltage-dependent manner. On the other hand, the current amplitude reduction induced by muscarinic and GABA B receptor activation, was not relieved by a 50-ms conditioning prepulse to +50 mV. This suggests the possibility of an alternative voltage-independent modulation mechanism.
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