Literature DB >> 7532338

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

B Hille1.   

Abstract

Neurotransmitters acting through G-protein-coupled receptors change the electrical excitability of neurons. Activation of receptors can affect the voltage dependence, the speed of gating, and the probability of opening of various ion channels, thus changing the computational state and outputs of a neuron. Each cell expresses many kinds of receptors, and uses several intracellular signaling pathways to modulate channel function in different ways. It has become possible to dissect these pathways by combining pharmacological and biophysical experiments. Recent patch-clamp work in sympathetic neurons will be summarized to illustrate the mechanisms underlying modulation and its significance.

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Year:  1994        PMID: 7532338     DOI: 10.1016/0166-2236(94)90157-0

Source DB:  PubMed          Journal:  Trends Neurosci        ISSN: 0166-2236            Impact factor:   13.837


  253 in total

1.  Decreased G-protein-mediated regulation and shift in calcium channel types with age in hippocampal cultures.

Authors:  E M Blalock; N M Porter; P W Landfield
Journal:  J Neurosci       Date:  1999-10-01       Impact factor: 6.167

2.  Implications of G-protein-mediated Ca2+ channel inhibition for neurotransmitter release and facilitation.

Authors:  R Bertram; M Behan
Journal:  J Comput Neurosci       Date:  1999 Nov-Dec       Impact factor: 1.621

3.  Allosteric modulation of Ca2+ channels by G proteins, voltage-dependent facilitation, protein kinase C, and Ca(v)beta subunits.

Authors:  S Herlitze; H Zhong; T Scheuer; W A Catterall
Journal:  Proc Natl Acad Sci U S A       Date:  2001-04-10       Impact factor: 11.205

4.  Control of gating mode by a single amino acid residue in transmembrane segment IS3 of the N-type Ca2+ channel.

Authors:  H Zhong; B Li; T Scheuer; W A Catterall
Journal:  Proc Natl Acad Sci U S A       Date:  2001-04-10       Impact factor: 11.205

5.  Biphasic, opposing modulation of cloned neuronal alpha1E Ca channels by distinct signaling pathways coupled to M2 muscarinic acetylcholine receptors.

Authors:  U Meza; R Bannister; K Melliti; B Adams
Journal:  J Neurosci       Date:  1999-08-15       Impact factor: 6.167

6.  betagamma dimers derived from Go and Gi proteins contribute different components of adrenergic inhibition of Ca2+ channels in rat sympathetic neurones.

Authors:  P Delmas; F C Abogadie; G Milligan; N J Buckley; D A Brown
Journal:  J Physiol       Date:  1999-07-01       Impact factor: 5.182

7.  Multiple G-protein betagamma combinations produce voltage-dependent inhibition of N-type calcium channels in rat superior cervical ganglion neurons.

Authors:  V Ruiz-Velasco; S R Ikeda
Journal:  J Neurosci       Date:  2000-03-15       Impact factor: 6.167

8.  Heteromeric assembly of GABA(B)R1 and GABA(B)R2 receptor subunits inhibits Ca(2+) current in sympathetic neurons.

Authors:  A K Filippov; A Couve; M N Pangalos; F S Walsh; D A Brown; S J Moss
Journal:  J Neurosci       Date:  2000-04-15       Impact factor: 6.167

9.  Reluctant gating of single N-type calcium channels during neurotransmitter-induced inhibition in bullfrog sympathetic neurons.

Authors:  H K Lee; K S Elmslie
Journal:  J Neurosci       Date:  2000-05-01       Impact factor: 6.167

10.  Endogenous regulator of G-protein signaling proteins modify N-type calcium channel modulation in rat sympathetic neurons.

Authors:  S W Jeong; S R Ikeda
Journal:  J Neurosci       Date:  2000-06-15       Impact factor: 6.167

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