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Frederique Scamps - One of the best experts on this subject based on the ideXlab platform.
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calcium activated Chloride Current expression in axotomized sensory neurons what for
Frontiers in Molecular Neuroscience, 2012Co-Authors: Mathieu Boudes, Frederique ScampsAbstract:Calcium-activated Chloride Currents (CaCCs) are activated by an increase in intracellular calcium concentration. Peripheral nerve injury induces the expression of CaCCs in a subset of adult sensory neurons in primary culture including mechano- and proprioceptors, though not nociceptors. Functional screenings of potential candidate genes established that Best1 is a molecular determinant for CaCC expression among axotomized sensory neurons, while Tmem16a is acutely activated by inflammatory mediators in nociceptors. In nociceptors, such CaCCs are preferentially activated under receptor-induced calcium mobilization contributing to cell excitability and pain. In axotomized mechano- and proprioceptors, CaCC activation does not promote electrical activity and prevents firing, a finding consistent with electrical silencing for growth competence of adult sensory neurons. In favor of a role in the process of neurite growth, CaCC expression is temporally correlated to neurons displaying a regenerative mode of growth. This perspective focuses on the molecular identity and role of CaCC in axotomized sensory neurons and the future directions to decipher the cellular mechanisms regulating CaCC during neurite (re)growth.
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expression of three distinct families of calcium activated Chloride channel genes in the mouse dorsal root ganglion
Neuroscience Bulletin, 2007Co-Authors: Mohammed Aljumaily, Jean Valmier, Frederique Scamps, Alexei Kozlenkov, Ilana Mechaly, Agnes Fichard, Valerie Matha, Patrick CarrollAbstract:Objective A calcium-activated Chloride Current (I Cl(Ca)) has been observed in medium-sized sensory neurons of the dorsal root ganglion (DRG). Axotomy of the sciatic nerve induces a similar Current in the majority of medium and large diameter neurons. Our aim is to identify the molecule(s) underlying this Current.
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k Current regulates calcium activated Chloride Current induced afterdepolarization in axotomized sensory neurons
European Journal of Neuroscience, 2005Co-Authors: Cecile Hilaire, Sylvain Andre, Brice Campo, Jean Valmier, Frederique ScampsAbstract:One of the major electrophysiological effects of axotomy is a hyperexcitability of injured afferents that is thought to be involved in peripheral neuropathic pain. The molecular determinants of injured sensory neuron excitability are complex and not all have been identified. We have previously shown that sciatic nerve section upregulates the Ca(2+)-activated Cl(-) Current in subsets of medium and large sensory neurons. In the peripheral nervous system, the Ca(2+)-activated Cl(-) Current can promote after depolarization (ADP) and may therefore be involved in excitability. In this study, we set the conditions for Ca(2+)-activated Cl(-) Current activation during the electrical activity of axotomized sensory neurons. We used the whole-cell patch-clamp technique and Ca(2+) fluorescence measurements to record electrical activity or ionic Currents associated with intracellular Ca(2+) transients. An analysis of Ca(2+) fluorescence variation under Ca(2+)-activated Cl(-) Current activation showed that the Ca(2+) sensitivity of the Ca(2+)-activated Cl(-) Current did not allow activation upon one action potential (AP) but instead necessitated intracellular Ca(2+) loading under high-frequency electrical activity or AP lengthening. Nevertheless, ADP was exclusively recorded under AP lengthening following K(+) Current inhibition with either extracellular tetraethylammonium or intracellular Cs(+). The measurement of APs and ionic Currents associated with the use of niflumic acid to inhibit Cl(-) Currents showed that the Ca(2+)-activated Cl(-) Current was responsible for the ADP observed during K(+) Current inhibition. Thus, the Ca(2+)-activated Cl(-) Current-induced ADP in axotomized sensory neurons is regulated by K(+) Current density.
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axotomy induced expression of calcium activated Chloride Current in subpopulations of mouse dorsal root ganglion neurons
Journal of Neurophysiology, 2003Co-Authors: Sylvain Andre, Hassan Boukhaddaoui, Brice Campo, Mohammed Aljumaily, Veronique Mayeux, Denis Greuet, Jean Valmier, Frederique ScampsAbstract:Whole cell patch-clamp recordings of calcium-activated Chloride Current [ICl(Ca)] were made from adult sensory neurons of naive and axotomized mouse L4–L6 lumbar dorsal root ganglia after 1 day of ...
Steve Sorota - One of the best experts on this subject based on the ideXlab platform.
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cardiac swelling induced Chloride Current depolarizes canine atrial myocytes
American Journal of Physiology-heart and Circulatory Physiology, 1997Co-Authors: Steve SorotaAbstract:The effect of the cardiac swelling-induced Chloride Current (I(Cl,swell)) on the transmembrane potential was examined. Osmotic swelling affected the resting potassium Current through an apparent dilution of intracellular potassium. Inflating cells by applying positive pressure to the patch electrode prevented the effect on the resting potassium Current. Inflation depolarized dog atrial myocytes when the recording electrodes contained either 17 or 42 mM Cl-. The depolarization coincided with activation of I(Cl,swell) and was antagonized by the Chloride-channel blocker niflumic acid. Substituting extracellular Chloride with the more permeant ion SCN- shifted the reversal potential for I(Cl,swell) to more negative values and antagonized inflation-induced depolarization. The depolarization was accentuated by replacing extracellular Chloride with a less permeant ion, aspartate. We conclude that activation of I(Cl,swell) in atrial cells causes significant depolarization of the resting membrane. The outward rectification of I(Cl,swell) and the high cell membrane resistance during the action potential plateau suggest that I(Cl,swell) will also have significant effects on atrial action potential configuration.
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tyrosine protein kinase inhibitors prevent activation of cardiac swelling induced Chloride Current
Pflügers Archiv: European Journal of Physiology, 1995Co-Authors: Steve SorotaAbstract:The effect of tyrosine protein kinase inhibitors on the swelling-induced Chloride Current (ICl-swelling of dog atrial myocytes was studied using the whole-cell patch-clamp recording technique. Currents were measured during hyperpolarizing voltage ramps with potassium Currents blocked by cesium. Osmolarity was varied using mannitol. Exposure to hypotonic solution (≈249 mosmol/kg) activated ICl-swelling. Hypertonic solution (≈ 363mosmol/kg) was used to shrink swollen cells and turn off ICl-swelling. In studies on the acute effect of tyrosine protein kinase inhibitors each cell was swollen three separate times. Control, treatment, and washout ICl-swelling were compared. Genistein (50–80 μM) prevented reactivation of ICl-swelling without affecting cell size. The effect of genistein partially subsided upon washout. The effect of genistein on ICl-swelling was not mimicked by 80 μM daidzein, a related compound that does not inhibit tyrosine protein kinases. When intracellular adenosine 5′-0-(3-thiotriphosphate (ATP[γS]) was used, genistein did not prevent the reactivation of ICl-swelling. Intracellular ATP[γS] did not result in a persistent activation of ICl-swelling when cell size was returned to control. Acute exposure to 1 μM herbimycin A or 100 μM tyrphostin 51 did not prohibit the activation of ICl-swelling. A 24-h exposure to 1 μM herbimycin A did inhibit ICl-swelling. The results provide important clues regarding the activation mechanism for ICl-swelling and suggest that a tyrosine protein phosphorylation may be necessary, but not sufficient, for activation of ICl-swelling.
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forskolin stimulates swelling induced Chloride Current not cardiac cystic fibrosis transmembrane conductance regulator Current in human cardiac myocytes
Circulation Research, 1995Co-Authors: Steve SorotaAbstract:Abstract Whole-cell patch clamp was used to look for cystic fibrosis transmembrane-conductance regulator (CFTR)–like Chloride Currents in calcium-tolerant human cardiac myocytes. Potassium-containing solutions were used initially. Steady state Currents were measured with hyperpolarizing ramps (−16.25 mV/s). Peak net inward Currents during voltage steps from −50 to +5 mV were used as an index of L-type calcium Current. Isoproterenol (1 μmol/L) or forskolin (10 μmol/L) were used in attempts to evoke CFTR-like Chloride Current. No forskolin- or isoproterenol-induced steady state Current was found in any of 17 atrial cells from seven patients in the absence of cell swelling. Every cell exhibited a large increase in net inward Current in response to forskolin, suggesting that cAMP-dependent stimulation of L-type calcium Current was present. Swelling with osmotic stress induced an outwardly rectifying steady state Current with a reversal potential close to the Chloride equilibrium potential. Once this Current w...
Jean Valmier - One of the best experts on this subject based on the ideXlab platform.
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expression of three distinct families of calcium activated Chloride channel genes in the mouse dorsal root ganglion
Neuroscience Bulletin, 2007Co-Authors: Mohammed Aljumaily, Jean Valmier, Frederique Scamps, Alexei Kozlenkov, Ilana Mechaly, Agnes Fichard, Valerie Matha, Patrick CarrollAbstract:Objective A calcium-activated Chloride Current (I Cl(Ca)) has been observed in medium-sized sensory neurons of the dorsal root ganglion (DRG). Axotomy of the sciatic nerve induces a similar Current in the majority of medium and large diameter neurons. Our aim is to identify the molecule(s) underlying this Current.
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k Current regulates calcium activated Chloride Current induced afterdepolarization in axotomized sensory neurons
European Journal of Neuroscience, 2005Co-Authors: Cecile Hilaire, Sylvain Andre, Brice Campo, Jean Valmier, Frederique ScampsAbstract:One of the major electrophysiological effects of axotomy is a hyperexcitability of injured afferents that is thought to be involved in peripheral neuropathic pain. The molecular determinants of injured sensory neuron excitability are complex and not all have been identified. We have previously shown that sciatic nerve section upregulates the Ca(2+)-activated Cl(-) Current in subsets of medium and large sensory neurons. In the peripheral nervous system, the Ca(2+)-activated Cl(-) Current can promote after depolarization (ADP) and may therefore be involved in excitability. In this study, we set the conditions for Ca(2+)-activated Cl(-) Current activation during the electrical activity of axotomized sensory neurons. We used the whole-cell patch-clamp technique and Ca(2+) fluorescence measurements to record electrical activity or ionic Currents associated with intracellular Ca(2+) transients. An analysis of Ca(2+) fluorescence variation under Ca(2+)-activated Cl(-) Current activation showed that the Ca(2+) sensitivity of the Ca(2+)-activated Cl(-) Current did not allow activation upon one action potential (AP) but instead necessitated intracellular Ca(2+) loading under high-frequency electrical activity or AP lengthening. Nevertheless, ADP was exclusively recorded under AP lengthening following K(+) Current inhibition with either extracellular tetraethylammonium or intracellular Cs(+). The measurement of APs and ionic Currents associated with the use of niflumic acid to inhibit Cl(-) Currents showed that the Ca(2+)-activated Cl(-) Current was responsible for the ADP observed during K(+) Current inhibition. Thus, the Ca(2+)-activated Cl(-) Current-induced ADP in axotomized sensory neurons is regulated by K(+) Current density.
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axotomy induced expression of calcium activated Chloride Current in subpopulations of mouse dorsal root ganglion neurons
Journal of Neurophysiology, 2003Co-Authors: Sylvain Andre, Hassan Boukhaddaoui, Brice Campo, Mohammed Aljumaily, Veronique Mayeux, Denis Greuet, Jean Valmier, Frederique ScampsAbstract:Whole cell patch-clamp recordings of calcium-activated Chloride Current [ICl(Ca)] were made from adult sensory neurons of naive and axotomized mouse L4–L6 lumbar dorsal root ganglia after 1 day of ...
Mohammed Aljumaily - One of the best experts on this subject based on the ideXlab platform.
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expression of three distinct families of calcium activated Chloride channel genes in the mouse dorsal root ganglion
Neuroscience Bulletin, 2007Co-Authors: Mohammed Aljumaily, Jean Valmier, Frederique Scamps, Alexei Kozlenkov, Ilana Mechaly, Agnes Fichard, Valerie Matha, Patrick CarrollAbstract:Objective A calcium-activated Chloride Current (I Cl(Ca)) has been observed in medium-sized sensory neurons of the dorsal root ganglion (DRG). Axotomy of the sciatic nerve induces a similar Current in the majority of medium and large diameter neurons. Our aim is to identify the molecule(s) underlying this Current.
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axotomy induced expression of calcium activated Chloride Current in subpopulations of mouse dorsal root ganglion neurons
Journal of Neurophysiology, 2003Co-Authors: Sylvain Andre, Hassan Boukhaddaoui, Brice Campo, Mohammed Aljumaily, Veronique Mayeux, Denis Greuet, Jean Valmier, Frederique ScampsAbstract:Whole cell patch-clamp recordings of calcium-activated Chloride Current [ICl(Ca)] were made from adult sensory neurons of naive and axotomized mouse L4–L6 lumbar dorsal root ganglia after 1 day of ...
Michaela Kress - One of the best experts on this subject based on the ideXlab platform.
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Identification of Chloride Channels CLCN3 and CLCN5 Mediating the Excitatory Cl− Currents Activated by Sphingosine-1-Phosphate in Sensory Neurons
Frontiers in molecular neuroscience, 2018Co-Authors: Norbert Mair, Kai K. Kummer, Michael G. Leitner, María Camprubí-robles, Michiel Langeslag, Michaela KressAbstract:Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid involved in numerous physiological and pathophysiological processes. We have previously reported a S1P-induced nocifensive response in mice by excitation of sensory neurons via activation of an excitatory Chloride Current. The underlying molecular mechanism for the S1P-induced Chloride conductance remains elusive. In the present study, we identified two CLCN voltage-gated Chloride channels, CLCN3 and CLCN5, which mediated a S1P-induced excitatory Cl- Current in sensory neurons by combining RNA-seq, adenovirus-based gene silencing and whole-cell electrophysiological voltage-clamp recordings. Downregulation of CLCN3 and CLCN5 channels by adenovirus-mediated delivery of shRNA dramatically reduced S1P-induced Cl- Current and membrane depolarization in sensory neurons. The mechanism of S1P-induced activation of the Chloride Current involved Rho GTPase but not Rho-associated protein kinase. Although S1P-induced potentiation of TRPV1-mediated ionic Currents also involved Rho-dependent process, the lack of correlation of the S1P-activated Cl- Current and the potentiation of TRPV1 by S1P suggests that CLCN3 and CLCN5 are necessary components for S1P-induced excitatory Cl- Currents but not for the amplification of TRPV1-mediated Currents in sensory neurons. This study provides a novel mechanistic insight into the importance of bioactive sphingolipids in nociception.
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identification of Chloride channels clcn3 and clcn5 mediating the excitatory cl Currents activated by sphingosine 1 phosphate in sensory neurons
Frontiers in Molecular Neuroscience, 2018Co-Authors: Norbert Mair, Kai K. Kummer, Michael G. Leitner, Michiel Langeslag, Maria Camprubirobles, Michaela KressAbstract:Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid involved in numerous physiological and pathophysiological processes. We have previously reported a S1P-induced nocifensive response in mice by excitation of sensory neurons via activation of an excitatory Chloride Current. The underlying molecular mechanism for the S1P-induced Chloride conductance remains elusive. In the present study, we identified two CLCN voltage-gated Chloride channels, CLCN3 and CLCN5, which mediated a S1P-induced excitatory Cl- Current in sensory neurons by combining RNA-seq, adenovirus-based gene silencing and whole-cell electrophysiological voltage-clamp recordings. Downregulation of CLCN3 and CLCN5 channels by adenovirus-mediated delivery of shRNA dramatically reduced S1P-induced Cl- Current and membrane depolarization in sensory neurons. The mechanism of S1P-induced activation of the Chloride Current involved Rho GTPase but not Rho-associated protein kinase. Although S1P-induced potentiation of TRPV1-mediated ionic Currents also involved Rho-dependent process, the lack of correlation of the S1P-activated Cl- Current and the potentiation of TRPV1 by S1P suggests that CLCN3 and CLCN5 are necessary components for S1P-induced excitatory Cl- Currents but not for the amplification of TRPV1-mediated Currents in sensory neurons. This study provides a novel mechanistic insight into the importance of bioactive sphingolipids in nociception.