6533b820fe1ef96bd127913a

RESEARCH PRODUCT

Differential blockade by nifedipine and ω-conotoxin GVIA of α1- and β1-adrenoceptor-controlled calcium channels on motor nerve terminals of the rat

Hartmut OsswaldFriederike SchlemmerDavid J. DooleyIgnaz Wessler

subject

medicine.medical_specialtyNifedipineNeuromuscular JunctionMollusk Venomschemistry.chemical_elementIn Vitro TechniquesCalciumN-type calcium channelMotor Endplatecomplex mixturesNeuromuscular junctionNifedipineomega-Conotoxin GVIAInternal medicinemedicineAnimalsL-type calcium channelVoltage-dependent calcium channelChemistryGeneral NeuroscienceCalcium channelRats Inbred StrainsCalcium Channel BlockersAcetylcholineElectric StimulationRatsReceptors AdrenergicPhrenic Nervemedicine.anatomical_structureEndocrinologyCalcium ChannelsAcetylcholinemedicine.drug

description

Electrically evoked release of [3H]acetylcholine ([3H]ACh) from the rat phrenic nerve and its facilitation by stimulation of presynaptic alpha 1- and beta 1-adrenoceptors were investigated in the absence and presence of nifedipine and omega-conotoxin GVIA. Both calcium channel antagonists did not modify electrically evoked [3H]ACh release, but selectively blocked the effect triggered by both facilitatory adrenergic receptors. The increase in [3H]ACh release mediated via beta 1-adrenoceptor activation was abolished by low concentrations (1 nM) of omega-conotoxin GVIA, whereas nifedipine (100 nM) abolished the facilitatory effect mediated via alpha 1-adrenoceptor stimulation. Therefore, the beta 1-adrenoceptor is apparently coupled to a calcium channel that can be regarded as of the N-type, and the alpha 1-adrenoceptor is apparently coupled to a calcium channel that appears as a subtype of the L-type which is not sensitive to omega-conotoxin GVIA.

yearjournalcountryeditionlanguage
1990-01-01Neuroscience Letters
https://doi.org/10.1016/0304-3940(90)90726-p