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Membrane currents and cytoplasmic sodium transients generated by glutamate transport in Bergmann glial cells.
Pflugers Arch. 2007 May; 454(2):245-52.PA

Abstract

Effects of glutamate and kainate (KA) on Bergmann glial cells were investigated in mouse cerebellar slices using the whole-cell configuration of the patch-clamp technique combined with SBFI-based Na(+) microfluorimetry. L-glutamate (1 mM) and KA (100 microM) induced inward currents in Bergmann glial cells voltage-clamped at -70 mV. These currents were accompanied by an increase in intracellular Na+ concentration ([Na+](i)) from the average resting level of 5.2 +/- 0.5 mM to 26 +/- 5 mM and 33 +/- 7 mM, respectively. KA-evoked signals (1) were completely blocked in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM), an antagonist of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/KA ionotropic glutamate receptors; (2) reversed at 0 mV, and (3) disappeared in Na+ -free, N-methyl-D-glucamine (NMDG+)-containing solution, but remained almost unchanged in Na+ -free, Li+ -containing solution. Conversely, L-glutamate-induced signals (1) were marginally CNQX sensitive (approximately 10% inhibition), (2) did not reverse at a holding potential of +20 mV, (3) were markedly suppressed by Na+ substitution with both NMDG+ and Li+, and (4) were inhibited by D,L-threo-beta-benzyloxyaspartate. Further, D-glutamate, L -, and D-aspartate were also able to induce Na+ -dependent inward current. Stimulation of parallel fibres triggered inward currents and [Na+](i) transients that were insensitive to CNQX and MK-801; hence, we suggested that synaptically released glutamate activates glutamate/Na+ transporter in Bergmann glial cells, which produces a substantial increase in intracellular Na+ concentration.

Authors+Show Affiliations

Kirischuk S
Max-Delbruck-Centre for Molecular Medicine, Robert-Rossle-Strasse 10, 13122 Berlin-Buch, Germany.
Kettenmann H
No affiliation info available
Verkhratsky A
No affiliation info available

MeSH

6-Cyano-7-nitroquinoxaline-2,3-dioneAmino Acid Transport System X-AGAnimalsAspartic AcidCalciumCerebellumCytoplasmDizocilpine MaleateElectric StimulationElectrophysiologyExcitatory Amino Acid AntagonistsGlucosamineGlutamic AcidKainic AcidLithiumMembrane PotentialsMiceMice, Inbred StrainsModels, BiologicalNerve FibersNeurogliaSodiumSodium-Calcium Exchanger

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17273865

Citation

Kirischuk, Sergei, et al. "Membrane Currents and Cytoplasmic Sodium Transients Generated By Glutamate Transport in Bergmann Glial Cells." Pflugers Archiv : European Journal of Physiology, vol. 454, no. 2, 2007, pp. 245-52.
Kirischuk S, Kettenmann H, Verkhratsky A. Membrane currents and cytoplasmic sodium transients generated by glutamate transport in Bergmann glial cells. Pflugers Arch. 2007;454(2):245-52.
Kirischuk, S., Kettenmann, H., & Verkhratsky, A. (2007). Membrane currents and cytoplasmic sodium transients generated by glutamate transport in Bergmann glial cells. Pflugers Archiv : European Journal of Physiology, 454(2), 245-52.
Kirischuk S, Kettenmann H, Verkhratsky A. Membrane Currents and Cytoplasmic Sodium Transients Generated By Glutamate Transport in Bergmann Glial Cells. Pflugers Arch. 2007;454(2):245-52. PubMed PMID: 17273865.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Membrane currents and cytoplasmic sodium transients generated by glutamate transport in Bergmann glial cells. AU - Kirischuk,Sergei, AU - Kettenmann,Helmut, AU - Verkhratsky,Alexei, Y1 - 2007/02/02/ PY - 2007/01/04/received PY - 2007/01/06/accepted PY - 2007/2/3/pubmed PY - 2007/8/7/medline PY - 2007/2/3/entrez SP - 245 EP - 52 JF - Pflugers Archiv : European journal of physiology JO - Pflugers Arch VL - 454 IS - 2 N2 - Effects of glutamate and kainate (KA) on Bergmann glial cells were investigated in mouse cerebellar slices using the whole-cell configuration of the patch-clamp technique combined with SBFI-based Na(+) microfluorimetry. L-glutamate (1 mM) and KA (100 microM) induced inward currents in Bergmann glial cells voltage-clamped at -70 mV. These currents were accompanied by an increase in intracellular Na+ concentration ([Na+](i)) from the average resting level of 5.2 +/- 0.5 mM to 26 +/- 5 mM and 33 +/- 7 mM, respectively. KA-evoked signals (1) were completely blocked in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM), an antagonist of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/KA ionotropic glutamate receptors; (2) reversed at 0 mV, and (3) disappeared in Na+ -free, N-methyl-D-glucamine (NMDG+)-containing solution, but remained almost unchanged in Na+ -free, Li+ -containing solution. Conversely, L-glutamate-induced signals (1) were marginally CNQX sensitive (approximately 10% inhibition), (2) did not reverse at a holding potential of +20 mV, (3) were markedly suppressed by Na+ substitution with both NMDG+ and Li+, and (4) were inhibited by D,L-threo-beta-benzyloxyaspartate. Further, D-glutamate, L -, and D-aspartate were also able to induce Na+ -dependent inward current. Stimulation of parallel fibres triggered inward currents and [Na+](i) transients that were insensitive to CNQX and MK-801; hence, we suggested that synaptically released glutamate activates glutamate/Na+ transporter in Bergmann glial cells, which produces a substantial increase in intracellular Na+ concentration. SN - 0031-6768 UR - https://www.unboundmedicine.com/medline/citation/17273865/Membrane_currents_and_cytoplasmic_sodium_transients_generated_by_glutamate_transport_in_Bergmann_glial_cells_ L2 - https://dx.doi.org/10.1007/s00424-007-0207-5 DB - PRIME DP - Unbound Medicine ER -