Modulation of ion-channel function by G-protein-coupled receptors

Hille, Bertil

doi:10.1016/0166-2236(94)90157-0

Cited by 720 publications

(711 citation statements)

References 63 publications

Supporting

Mentioning

675

Contrasting

Unclassified

Order By: Relevance

“…The VD-mode inhibition is mediated by a rapid "membrane delimited" pathway, probably involving the interaction of G-protein βγ subunits with the VDCCs (Ikeda, 1996;Herlitze et al, 1996;Diversé-Pierluissi et al, 1995). Whereas, the VI-mode inhibition is generally thought to involve a diffusible second messenger (Bernheim et al, 1991;Hille, 1994). In this study, we demonstrated that NPY produced a typical VD-mode inhibition of IBa characterized by kinetic slowed and relieved by strong depolarizing voltage prepulse (Fig 5).…”

Section: Discussionsupporting

confidence: 56%

Neuropeptide Y modulates calcium channels in hamster submandibular ganglion neurons

Endoh

Nobushima

Tazaki

2012

Neuroscience Research

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 56%

Neuropeptide Y modulates calcium channels in hamster submandibular ganglion neurons

Endoh

Nobushima

Tazaki

2012

Neuroscience Research

View full text Add to dashboard Cite

“…administration of PTX (Galeotti et al 1996(Galeotti et al , 1997. PTX-sensitive Gproteins (G i ) are responsible for modulation of ionic conductance through a direct interaction with the ion channel and/or by lowering intracellular cyclic AMP levels (Hille, 1994). The K ATP channels can be opened through a mechanism mediated by G-proteins.…”

Section: Discussionmentioning

confidence: 99%

“…Other K + channels can be modulated by neurotransmitters interacting with Gprotein-coupled receptors (Brown and Birnbaumer, 1990;Brown, 1990). G proteins can modulate different types of K + channels through a direct effect on the ion channel or through an enzymatic step leading to the generation of cytoplasmic second messengers (Brown, 1990;Hille, 1994). Various pharmacological compounds can modulate these channels.…”

mentioning

confidence: 99%

Involvement of potassium channels in amitriptyline and clomipramine analgesia

2001

View full text Add to dashboard Cite

The effect of the administration of modulators of different subtypes of K + channels on antinociception induced by the tricyclic antidepressants amitriptyline and clomipramine was evaluated in the mouse hot plate test. The administration of the voltage-gated K + channel blocker tetraethylammonium (0.01-0.5 µg per mouse i.c.v.) prevented antinociception induced by both amitriptyline (15 mg kg Ϫ1 s.c.) and clomipramine (25 mg kg Ϫ1 s.c.). The K ATP channel blocker gliquidone (0.1-1.0 µg per mouse i.c.v.) prevented antinociception produced by amitriptyline and clomipramine whereas the K ATP channel openers minoxidil (10 µg per mouse i.c.v.) and pinacidil (25 µg per mouse i.c.v.) potentiated tricyclic antidepressant-induced analgesia. The administration of the Ca 2+ -gated K + channel blocker apamin (0.1-1.0 ng per mouse i.c.v.) completely prevented amitriptyline and clomipramine analgesia. At the highest effective doses, none of the drugs used induced behavioural side effects or impaired motor coordination, as revealed by the rota-rod test, spontaneous motility or inspection activity, as revealed by the hole board test. The present results demonstrate that central antinociception induced by amitriptyline and clomipramine involves the opening of different subtypes of K + channels (voltage-gated, K ATP and Ca 2+ -gated) which, therefore, represent a step in the transduction mechanism of tricyclic antidepressant analgesia.

show abstract

“…Therefore, it is possible that modulation of I Ca by the activation of the D 2 receptor occurs through membrane-delimited mechanisms. 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].…”

Section: Discussionmentioning

confidence: 99%

“…The mechanism that couples the D 2 receptor to Ca 2+ channels is not well understood, but several studies point to the involvement of G i/o proteins that are sensitive to pertussin toxin (PTX) [12,16,27,36]. We know that PC12 cells adapt to prolonged exposure to hypoxia with a series of events such as increased responsiveness to acute exposure to hypoxia [5,23,34] and increased tyrosine hydroxylase gene expression [6,30].…”

Section: Introductionmentioning

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

View full text Add to dashboard Cite

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.

show abstract

Modulation of ion-channel function by G-protein-coupled receptors

Cited by 720 publications

References 63 publications

Neuropeptide Y modulates calcium channels in hamster submandibular ganglion neurons

Neuropeptide Y modulates calcium channels in hamster submandibular ganglion neurons

Involvement of potassium channels in amitriptyline and clomipramine analgesia

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

Contact Info

Product

Resources

About