European Journal of Pharmacology: Molecular Pharmacology
Norepinephrine inhibits a Ca2+ current in rat sympathetic neurons via a G-protein
References (36)
- et al.
Regulation of hormone receptors and adenylyl cyclases by guanine nucleotide binding N proteins
Recent Prog. Horm. Res.
(1985) - et al.
Guanosine 5′-O-(2-thiodiphosphate): an inhibitor of adenylate cyclase stimulation by guanine nucleotides and fluoride ions
- et al.
Control of calcium current in rat sympathetic neurons by norepinephrine
Brain Res.
(1982) - et al.
Guanosine-5′-O-(3-thiotriphosphate) modifies kinetics of voltage dependent calcium current in chick sensory neurons
Biophys. J.
(1989) - et al.
Antibodies to the GTP binding protein, G0, antagonize norepinephrine-induced calcium current inhibition in NG108-15 hybrid cells
Neuron
(1989) - et al.
Specific inhibitors of protein kinase C block transmitter-induced modulation of sensory neuron calcium current
Neuron
(1989) - et al.
Regulation of adenylate cyclase of neuroblastoma × glioma hybrid cells by α-adrenergic receptors
J. Biol. Chem.
(1979) Norepinephrine blocks a calcium current of adult rat sympathetic neurons via an α2-adrenoceptor
European J. Pharmacol.
(1990)- et al.
Different GTP-binding proteins mediate regulation of calcium channels by acetylcholine and norepinephrine in rat sympathetic neurons
Brain Res.
(1989) - et al.
‘Concentration-clamp’ study of γ-aminobutyric-acid-induced chloride current kinetics in frog sensory neurons
J. Physiol. (London)
(1986)
Neurotransmitter inhibition of neuronal calcium currents by changes in channel voltage dependence
Nature
Muscarinic and α-adrenergic suppressions of calcium current (ICa) are blocked only partially by pertussis toxin in rat sympathetic neurons
Soc. Neurosci Abstracts
Mechanism of adenylate cyclase activation by cholera toxin: inhibition of GTP hydrolysis at the regulatory site
Role of guanine nucleotide binding protein in the activation of polyphosphoinositide phosphodiesterase
Nature
Calcium channel currents and their inhibition by (−)-baclofen in rat sensory neurons: modulation by guanine nucleotides
J. Physiol. (London)
Neurotransmitters decrease the calcium component of sensory neuron action potentials
Nature
Neurotransmitters decrease the calcium conductance activated by depolarization of embryonic chick sensory neurons
J. Physiol. (London)
Two types of calcium channels in the somatic membrane of new-born rat dorsal root ganglion neurons
J. Physiol. (London)
Cited by (34)
Phospholipase C-dependent hydrolysis of phosphatidylinositol 4,5-bisphosphate underlies agmatine-induced suppression of N-type Ca<sup>2+</sup> channel in rat celiac ganglion neurons
2017, Biochemical and Biophysical Research CommunicationsCitation Excerpt :Intracellular dialysis of GDPβS (2 mM) significantly attenuated agmatine-induced ICav2.2 inhibition (Fig. 1A and B). To elucidate the nature of G-protein involved in the agmatine-induced ICav2.2 inhibition, CG neurons were incubated for 16–18 h in a medium containing PTX (500 ng/mL), a potent inhibitor of heterotrimeric Gi/o protein [29–31]. Agmatine still inhibited ICav2.2 significantly with PTX pretreatment (Fig. 1C and D).
Modulation of N-type Ca<sup>2+</sup> currents by moxonidine via imidazoline I1 receptor activation in rat superior cervical ganglion neurons
2011, Biochemical and Biophysical Research CommunicationsCitation Excerpt :As shown in Supplementary Fig. 2, NE-induced Ca2+ inhibition displayed the hallmarks of voltage-dependent inhibition, namely kinetic slowing and prepulse facilitation or relief of current inhibition by conditioning depolarizing pulses. Prepulse facilitation, which is defined as the ratio of the postpulse to prepulse current amplitude, increased from 1.2 ± 0.36 to 1.6 ± 0.45 (p < 0.05, n = 6) after NE application (Supplementary Fig. 2, right), consistent with previous reports [27,29]. Meanwhile, moxonidine-induced ICa inhibition did not show any characteristics of voltage-dependent inhibition.
Activation of muscarinic m5 receptors inhibits recombinant KCNQ2/KCNQ3 K<sup>+</sup> channels expressed in HEK293T cells
2003, European Journal of Pharmacology