Neuron
ArticlePertussis toxin and voltage dependence distinguish multiple pathways modulating calcium channels of rat sympathetic neurons
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Cited by (174)
Regulation of neural ion channels by muscarinic receptors
2018, NeuropharmacologyCitation Excerpt :Marrion et al. (1987) first briefly reported that muscarine could inhibit a high voltage-activated Ca2+-current in dissociated adult sympathetic neurons. In a detailed study Wanke et al. (1987) showed that inhibition involved N-type (CaV2.2) channels; that it involved current slowing; that muscarinic inhibition was replicated and occluded by GTPγS [guanosine 5'-[y-thio]triphosphate], and hence involved a G-protein); that inhibition was prevented by pretreatment with Pertussis toxin; and that inhibition was independent of protein kinases A or C. Members of the Hille lab (Beech et al., 1992; Mathie et al., 1992; Bernheim et al., 1992) characterized the two forms of muscarinic inhibition of CaV2.2 channels in these neurons: M4Rs producing a rapid, voltage-dependent inhibition via a Pertussis-sensitive G-protein (much as described by Wanke et al., 1987, though then-incorrectly attributed by Wanke to M1Rs); and M1Rs producing a slow, voltage-independent, Pertussis-insensitive but intracellular Ca2+-dependent inhibition as described in 2.1.4 above; the latter involving a diffusible messenger but the former more direct. Subsequently Herlize et al. (1996), along with Ikeda (1996), showed that the βγ-subunits were responsible for the direct inhibition of CaV2 channels by noradrenaline in these neurons.
The role of P2Y<inf>1</inf> receptor signaling in central respiratory control
2016, Respiratory Physiology and NeurobiologyRegulation of Ca<inf>V</inf>2 calcium channels by G protein coupled receptors
2013, Biochimica et Biophysica Acta - BiomembranesPIP<inf>2</inf> hydrolysis is responsible for voltage independent inhibition of Ca<inf>V</inf>2.2 channels in sympathetic neurons
2013, Biochemical and Biophysical Research CommunicationsCitation Excerpt :This regulation is sensitive to calcium chelators such as BAPTA [17], is insensitive to toxins blocking Gαi/o proteins such as the toxin from Bordetella Pertussis [6,18], is slow and uses a diffusible second messenger [10], in contrast to the membrane delimited mechanism mediated by Gβγ subunits. This slow and PTX-insensitive pathway induced by muscarinic agonists seems to be similar to that described as voltage independent inhibition [6]. Whether these two pathways correspond to the same molecular cascade, it has not been firmly established.
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 Communications
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Present address: Department of Pharmacology, St. George's Hospital Medical School, Cranmer Terrace, London SW17 ORE, England.
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Present address: Département de Physiologie, Centre Medical Universitaire, 9 av. de Champel, 1211 Geneva, Switzerland.