Publications by authors named "Guyllaume Coiret"

4 Publications

  • Page 1 of 1

Neuron to astrocyte communication via cannabinoid receptors is necessary for sustained epileptiform activity in rat hippocampus.

PLoS One 2012 15;7(5):e37320. Epub 2012 May 15.

Brain Research Institute, University of Zurich, Zurich, Switzerland.

Astrocytes are integral functional components of synapses, regulating transmission and plasticity. They have also been implicated in the pathogenesis of epilepsy, although their precise roles have not been comprehensively characterized. Astrocytes integrate activity from neighboring synapses by responding to neuronally released neurotransmitters such as glutamate and ATP. Strong activation of astrocytes mediated by these neurotransmitters can promote seizure-like activity by initiating a positive feedback loop that induces excessive neuronal discharge. Recent work has demonstrated that astrocytes express cannabinoid 1 (CB1) receptors, which are sensitive to endocannabinoids released by nearby pyramidal cells. In this study, we tested whether this mechanism also contributes to epileptiform activity. In a model of 4-aminopyridine induced epileptic-like activity in hippocampal slice cultures, we show that pharmacological blockade of astrocyte CB1 receptors did not modify the initiation, but significantly reduced the maintenance of epileptiform discharge. When communication in astrocytic networks was disrupted by chelating astrocytic calcium, this CB1 receptor-mediated modulation of epileptiform activity was no longer observed. Thus, endocannabinoid signaling from neurons to astrocytes represents an additional significant factor in the maintenance of epileptiform activity in the hippocampus.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0037320PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3352897PMC
September 2012

Enhancement of CA3 hippocampal network activity by activation of group II metabotropic glutamate receptors.

Proc Natl Acad Sci U S A 2011 Jun 31;108(24):9993-7. Epub 2011 May 31.

Brain Research Institute, University of Zurich, CH-8057 Zurich, Switzerland.

Impaired function or expression of group II metabotropic glutamate receptors (mGluRIIs) is observed in brain disorders such as schizophrenia. This class of receptor is thought to modulate activity of neuronal circuits primarily by inhibiting neurotransmitter release. Here, we characterize a postsynaptic excitatory response mediated by somato-dendritic mGluRIIs in hippocampal CA3 pyramidal cells and in stratum oriens interneurons. The specific mGluRII agonists DCG-IV or LCCG-1 induced an inward current blocked by the mGluRII antagonist LY341495. Experiments with transgenic mice revealed a significant reduction of the inward current in mGluR3(-/-) but not in mGluR2(-/-) mice. The excitatory response was associated with periods of synchronized activity at theta frequency. Furthermore, cholinergically induced network oscillations exhibited decreased frequency when mGluRIIs were blocked. Thus, our data indicate that hippocampal responses are modulated not only by presynaptic mGluRIIs that reduce glutamate release but also by postsynaptic mGluRIIs that depolarize neurons and enhance CA3 network activity.
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http://dx.doi.org/10.1073/pnas.1100548108DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3116403PMC
June 2011

The antiestrogen tamoxifen activates BK channels and stimulates proliferation of MCF-7 breast cancer cells.

Mol Pharmacol 2007 Mar 12;71(3):843-51. Epub 2006 Dec 12.

Laboratoire de Physiologie Cellulaire et Moléculaire, EA 2086, Université Picardie Jules Verne, Faculté des Sciences, 33, Rue St Leu 80000 Amiens, France.

In the present study, we investigated the effect of the antiestrogen compound tamoxifen on BK channels by the use of the patch-clamp technique. The perfusion of 10 nM tamoxifen significantly increased the magnitude of a voltage-dependent K+ current by 22.6 +/- 10.6% (n = 23). The effect of tamoxifen was always obtained in the first minute, peaked at 5.9 +/- 2.2 min (n = 23), and was abolished by the perfusion of tetraethylammonium (0.5 mM), charybdotoxin (50 nM), or iberiotoxin (100 nM). The stimulatory effect of 10 nM tamoxifen was the same at low (50 nM) and high (700 nM) internal calcium concentration and was not additive to that of 17-beta-estradiol (E2) or its membrane-impermeant form, beta-estradiol 6-(O-carboxymethyl)oxime:bovine serum albumin. Furthermore, the effect of tamoxifen was still recorded in the presence of the selective estrogen receptor antagonist faslodex (ICI-182,780; 1 microM). At the single-channel level, tamoxifen significantly increased the open probability of the BK channel by 46.2 +/- 10.1% (n = 4) without changing its unitary conductance. Moreover, we show here that the stimulation of BK channel activity by tamoxifen is involved in MCF-7 cell proliferation. Taken together, these results permitted us to identify the BK channel as the molecular target of tamoxifen that probably acts at the same extracellular molecular level as E2. The site of action of tamoxifen is probably the channel itself or the auxiliary beta subunits.
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http://dx.doi.org/10.1124/mol.106.028290DOI Listing
March 2007

17-beta-estradiol activates maxi-K channels through a non-genomic pathway in human breast cancer cells.

FEBS Lett 2005 Jun;579(14):2995-3000

Laboratoire de Physiologie Cellulaire et Moléculaire, EA 2086, Université de Picardie Jules Verne, Faculté des Sciences, 33, Rue Saint-Leu 80039 Amiens, France.

We have investigated the acute effects of 17-beta-estradiol (E2) on K+ channels in MCF-7 breast epithelial cancer cells. E2 induced a rapid and irreversible augmentation of the K+ current for all membrane potentials superior to -25 mV. The effect of E2 was sensitive to Iberiotoxin, Charybdotoxin and TEA and can be elicited in the presence of the anti-estrogen ICI 182780 or be mimicked by the membrane impermeant form E2/BSA. Furthermore, E2/BSA was able to stimulate cell proliferation in a maxi-K inhibitors-sensitive manner. Thus, these results permit us to identify the maxi-K channel as the molecular target of E2 that regulates cell proliferation independently of the estrogen receptor.
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http://dx.doi.org/10.1016/j.febslet.2005.02.085DOI Listing
June 2005