Search results for "N-type calcium channel"

showing 2 items of 2 documents

Capsaicin differentially modulates voltage-activated calcium channel currents in dorsal root ganglion neurones of rats

2005

It is discussed whether capsaicin, an agonist of the pain mediating TRPV1 receptor, decreases or increases voltage-activated calcium channel (VACC) currents (ICa(V)). ICa(V) were isolated in cultured dorsal root ganglion (DRG) neurones of rats using the whole cell patch clamp method and Ba 2+ as charge carrier. In large diameter neurones (>35Am), a concentration of 50AM was needed to reduce ICa(V) (activated by depolarizations to 0 mV) by 80%, while in small diameter neurones (30Am), the IC50 was 0.36 AM. This effect was concentration dependent with a threshold below 0.025 AM and maximal blockade (>80%) at 5AM. The current–voltage relation was shifted to the hyperpolarized direction with an…

Pain ThresholdPatch-Clamp TechniquesTRPV1TRPV Cation ChannelsN-type calcium channelSecond Messenger SystemsMembrane PotentialsGanglia SpinalAnimalsL-type calcium channelPatch clampRats WistarMolecular BiologyCell SizeNeuronsDose-Response Relationship DrugVoltage-dependent calcium channelChemistryGeneral NeuroscienceCalcium channelT-type calcium channelCalciseptineAnatomyRatsRats Inbred LewBiophysicsCalcium ChannelsNeurology (clinical)CapsaicinSignal TransductionDevelopmental BiologyBrain Research
researchProduct

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

1990

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 b…

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.drugNeuroscience Letters
researchProduct