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Pharmacological and molecular characterization of glutamate receptors in the MIN6 pancreatic beta-cell line.
Neurol Res. 2000 Jun; 22(4):379-85.NR

Abstract

The MIN6 pancreatic beta-cell line responds to glutamate, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainate, but not N-methyl-D-aspartate (NMDA) or 1S,3R-trans-ACPD, with increases in [Ca2+]i. This correlates with MIN6 expression of AMPA receptor subunits (GluR1-4) but only weak expression of NMDA NR2 receptor subunits, as determined by reverse transcriptase polymerase chain reaction (RT-PCR). Pharmacological characterization of the MIN6 AMPA receptors showed that AMPA-triggered [Ca2+]i responses were blocked by GYKI 52466, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and pentobarbital. AMPA-triggered [Ca2+]i responses were also blocked in Na(+)-free medium and by the voltage-sensitive Ca2+ channel antagonist La3+. Unlike cortical neuronal cultures, which show a loss of membrane-associated protein kinase C (PKC) activity and die in response to excitatory amino acid exposure, glutamate was not toxic to MIN6 cells and it did not decrease PKC activity. These studies indicate that MIN6 cells possess Ca(2+)-impermeable AMPA receptors that secondarily allow Ca2+ influx following AMPA-induced depolarization and that, despite elevating [Ca2+]i, AMPA is not toxic to these cells. The effects of glutamate and glutamate receptor antagonists on pancreatic cells needs to be better understood if these compounds are to be used as therapeutic agents to treat stroke.

Authors+Show Affiliations

Institute for Biological Sciences, National Research Council of Canada, Ottawa, Ontario, Canada. paul.morley@nrc.caNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10874687

Citation

Morley, P, et al. "Pharmacological and Molecular Characterization of Glutamate Receptors in the MIN6 Pancreatic Beta-cell Line." Neurological Research, vol. 22, no. 4, 2000, pp. 379-85.
Morley P, MacLean S, Gendron TF, et al. Pharmacological and molecular characterization of glutamate receptors in the MIN6 pancreatic beta-cell line. Neurol Res. 2000;22(4):379-85.
Morley, P., MacLean, S., Gendron, T. F., Small, D. L., Tremblay, R., Durkin, J. P., & Mealing, G. (2000). Pharmacological and molecular characterization of glutamate receptors in the MIN6 pancreatic beta-cell line. Neurological Research, 22(4), 379-85.
Morley P, et al. Pharmacological and Molecular Characterization of Glutamate Receptors in the MIN6 Pancreatic Beta-cell Line. Neurol Res. 2000;22(4):379-85. PubMed PMID: 10874687.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Pharmacological and molecular characterization of glutamate receptors in the MIN6 pancreatic beta-cell line. AU - Morley,P, AU - MacLean,S, AU - Gendron,T F, AU - Small,D L, AU - Tremblay,R, AU - Durkin,J P, AU - Mealing,G, PY - 2000/6/30/pubmed PY - 2000/10/21/medline PY - 2000/6/30/entrez SP - 379 EP - 85 JF - Neurological research JO - Neurol Res VL - 22 IS - 4 N2 - The MIN6 pancreatic beta-cell line responds to glutamate, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainate, but not N-methyl-D-aspartate (NMDA) or 1S,3R-trans-ACPD, with increases in [Ca2+]i. This correlates with MIN6 expression of AMPA receptor subunits (GluR1-4) but only weak expression of NMDA NR2 receptor subunits, as determined by reverse transcriptase polymerase chain reaction (RT-PCR). Pharmacological characterization of the MIN6 AMPA receptors showed that AMPA-triggered [Ca2+]i responses were blocked by GYKI 52466, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and pentobarbital. AMPA-triggered [Ca2+]i responses were also blocked in Na(+)-free medium and by the voltage-sensitive Ca2+ channel antagonist La3+. Unlike cortical neuronal cultures, which show a loss of membrane-associated protein kinase C (PKC) activity and die in response to excitatory amino acid exposure, glutamate was not toxic to MIN6 cells and it did not decrease PKC activity. These studies indicate that MIN6 cells possess Ca(2+)-impermeable AMPA receptors that secondarily allow Ca2+ influx following AMPA-induced depolarization and that, despite elevating [Ca2+]i, AMPA is not toxic to these cells. The effects of glutamate and glutamate receptor antagonists on pancreatic cells needs to be better understood if these compounds are to be used as therapeutic agents to treat stroke. SN - 0161-6412 UR - https://www.unboundmedicine.com/medline/citation/10874687/Pharmacological_and_molecular_characterization_of_glutamate_receptors_in_the_MIN6_pancreatic_beta_cell_line_ DB - PRIME DP - Unbound Medicine ER -