Antibodies to the GTP binding protein, Go, antagonize noradrenaline-induced calcium current inhibition in NG108-15 hybrid cells

McFadzean, Ian; Mullaney, Ian; Brown, David A.; Milligan, Graeme

doi:10.1016/0896-6273(89)90030-5

Cited by 162 publications

(77 citation statements)

References 17 publications

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“…Since the unaffected Ba*+ peak current by cromakalim was inhibited by perfusion of acetylcholine as shown by McFadzean et al [12], the N-like current that was measured here was a responsible component.…”

Section: Resultssupporting

confidence: 64%

Cromakalim, a vasodilator, differentially inhibits Ca²⁺ currents in NG108‐15 neuroblastoma × glioma hybrid cells

et al. 1990

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Extracellular perfusion with the antihypertensive agent cromakalim produced an inhibition of 2266% in the low-threshold transient Ca*+ (T-like) current in NGIW15 hybrid cells. Cromakalim suppressed the ~gh-t~old and long-lasting Ba2+ current (L-like CaZ+ current) by 2973%, but had almost no effect on the hip-th~shold and inactivating B3+ current (N-like CaZ+ current). IC, for T-like and L-like currents was the same at about 100 PM. The inhibitory effect developed relatively fast and was reversible. These results indicate that cromakalim can selectively inhibit the activity of inward Ca*+ currents.

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Section: Resultssupporting

confidence: 64%

Cromakalim, a vasodilator, differentially inhibits Ca²⁺ currents in NG108‐15 neuroblastoma × glioma hybrid cells

et al. 1990

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“…We are currently examining the effect of dihydropyridines on GTPase in a purified reconstituted membrane system. Neurotransmitters inhibit voltage-dependent Ca "-+ channels in neurons and secretory cells via Go ( [4,[8][9][10]; see Introduction). The Ca ~-+ channel type which is modulated appears to be N-type in some neurons because of its sensitivity to omega-conotoxin, and because dihySepmmber 1992 dropyridine-agonist-enhanced tail currents do not display this modulation [2,231.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have demonstrated that a likely candidate for the subtype of G-protein involved is Go since reconstitution of purified Go into cells pretreated with pertussis toxin restores the inhibition of Ca -~" currents induced by receptor activation [4][5][6][7]. In addition, druginduced inhibition of Ca "~* currents is attenuated by anti-Go antibodies [5,8,9] and antisense oligonucleotides complementary to the mRNA of the g-subunit of Go [10]. In the latter case, the Ca a* current involved was identified as an L-type current [10] although non-L-type currents are also inhibited by neurotransmitters [2].…”

Section: Introductionmentioning

confidence: 99%

1,4‐Dihydropyridines modulate GTP hydrolysis by G_o in neuronal membranes

Sweeney

Dolphin

1992

FEBS Letters

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Several lines of evidence suggest that L-type Ca :~ channels (I ,4-dihydropyridin¢ receptors) are modulated by GTP-binding proteins. We have further examined this interaction by measuring the effect of 1,4-dihydropyridlnes on GTPase activity in brain membranes. Dihydropyridine agonists significantly increased GTPase, reflected by an increase in the maximal rate of GTP hydrolysis, without affecting the affinity for GTP or the binding ofa non-hydrolysable analogue of GTP.

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“…The activation is terminated by a GTPase activity intrinsic to the α-subunit. It is also widely accepted that G o α is primarily responsible for the modulation of neuronal voltage-dependent Ca 2+ channels [4,7,8,28], although several Gβγ subunits are able to transduce the signal to Ca 2+ channels [14,17]. We found that hypoxia induced an average decrease of about 25% in the levels of G i/o immunoreactivity.…”

Section: Discussionmentioning

confidence: 52%

“…Indeed, it is already established that membrane-delimited G protein regulation of Ca 2+ channels is common in neurons and that the G protein involved in this inhibition is PTX sensitive [7,12,16,36]. Growing evidence strongly implicates G o rather than G i in this regulation, which could also affect the suppression of neurotransmitter release that is mediated by receptors on presynaptic neurons [4,7,8,28]. Furthermore, membrane-delimited G protein regulation of I Ca by DA has been shown in chick sensory and sympathetic neurons [27].…”

Section: Discussionmentioning

confidence: 99%

Role of the D 2 dopamine receptor in molecular adaptation to chronic hypoxia in PC12 cells

Kobayashi¹,

Conforti²,

Zhu³

et al. 1999

Pfl�gers Archiv European Journal of Physiology

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We have previously shown that pheochromocytoma (PC12) cells rapidly depolarize and undergo Ca 2+ influx through voltage-dependent Ca 2+ channels in response to moderate hypoxia and that intracellular free Ca 2+ is modulated by activation of dopamine D 2 receptors in this cell type. The present study shows that D 2 (quinpirole-mediated) inhibition of a voltage-dependent Ca 2+ current (I Ca ) in PC12 cells is dramatically attenuated after chronic exposure to moderate hypoxia (24 h at 10% O 2 ). Pretreatment of cells with pertussis toxin abolished D 2 -mediated inhibition of I Ca . The D 2 -induced inhibition of I Ca did not depend on protein kinase A (PKA), as it persisted both in the presence of a specific PKA inhibitor (PKI) and in PKA-deficient PC12 cells. Prolonged exposure to hypoxia (24 h) significantly reduced the level of G i/o α immunoreactivity, but did not alter Gβ levels. Furthermore, dialysis of recombinant G o α protein through the patch pipette restored the inhibitory effect of quinpirole in cells chronically exposed to hypoxia. We conclude that the attenuation of the D 2 -mediated inhibition of I Ca by chronic hypoxia is caused by impaired receptor-G protein coupling, due to reduced levels of G o α protein. This attenuated feedback modulation of I Ca by dopamine may allow for a more sustained Ca 2+ influx and enhanced cellular excitation during prolonged hypoxia.

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Antibodies to the GTP binding protein, Go, antagonize noradrenaline-induced calcium current inhibition in NG108-15 hybrid cells

Cited by 162 publications

References 17 publications

Cromakalim, a vasodilator, differentially inhibits Ca²⁺ currents in NG108‐15 neuroblastoma × glioma hybrid cells

Cromakalim, a vasodilator, differentially inhibits Ca²⁺ currents in NG108‐15 neuroblastoma × glioma hybrid cells

1,4‐Dihydropyridines modulate GTP hydrolysis by G_o in neuronal membranes

Role of the D 2 dopamine receptor in molecular adaptation to chronic hypoxia in PC12 cells

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Antibodies to the GTP binding protein, Go, antagonize noradrenaline-induced calcium current inhibition in NG108-15 hybrid cells

Cited by 162 publications

References 17 publications

Cromakalim, a vasodilator, differentially inhibits Ca2+ currents in NG108‐15 neuroblastoma × glioma hybrid cells

Cromakalim, a vasodilator, differentially inhibits Ca2+ currents in NG108‐15 neuroblastoma × glioma hybrid cells

1,4‐Dihydropyridines modulate GTP hydrolysis by Go in neuronal membranes

Role of the D 2 dopamine receptor in molecular adaptation to chronic hypoxia in PC12 cells

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Cromakalim, a vasodilator, differentially inhibits Ca²⁺ currents in NG108‐15 neuroblastoma × glioma hybrid cells

Cromakalim, a vasodilator, differentially inhibits Ca²⁺ currents in NG108‐15 neuroblastoma × glioma hybrid cells

1,4‐Dihydropyridines modulate GTP hydrolysis by G_o in neuronal membranes