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The interactions between plasma membrane depolarization and glutamate receptor activation in the regulation of cytoplasmic free calcium in cultured cerebellar granule cells.
J Neurosci. 1990 Dec; 10(12):3873-9.JN

Abstract

The complex modulation of cytoplasmic free calcium concentration ([Ca2+]c) in primary cultures of cerebellar granule cells in response to glutamate receptor agonists has been the subject of several contradictory reports. We here show that 3 components of the [Ca2+]c response can be distinguished: (1) Ca2+ entry through voltage-dependent Ca2+ channels, following KCl- or receptor-evoked depolarization, (2) Ca2+ entry through NMDA receptor channels, and (3) liberation of internal Ca2+ via a metabolotropic receptor. Depolarization with KCl induced a transient [Ca2+]c response (subject to voltage inactivation) decaying to a sustained plateau (largely inhibited by nifedipine). The NMDA response was potentiated by glycine, totally inhibited by (+)5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801), and blocked by Mg2+ in a voltage-sensitive manner. Polarized cells displayed small responses to quisqualate (QA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA). Depolarization enhanced a transient response to QA, but not to AMPA. Trans-1-amino-1,3-cyclopentanedicarboxylic acid (trans-ACPD), a selective agonist for the metabolotropic glutamate receptor, caused a transient elevation of [Ca2+]c, which was blocked by prior exposure to QA but not AMPA. The prolonged [Ca2+]c response to kainate (KA) can be resolved into 2 major components: an indirect NMDA receptor-mediated response due to released glutamate and a nifedipine-sensitive component consistent with depolarization-mediated entry via Ca2+ channels. 6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX), QA at greater than 10 microM, and AMPA (but not trans-ACPD) reversed the KA response, consistent with an inactivation of the KA receptor.(

ABSTRACT

TRUNCATED AT 250 WORDS)

Authors+Show Affiliations

Department of Biochemistry, University of Dundee, Scotland, U.K.No affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

1980131

Citation

Courtney, M J., et al. "The Interactions Between Plasma Membrane Depolarization and Glutamate Receptor Activation in the Regulation of Cytoplasmic Free Calcium in Cultured Cerebellar Granule Cells." The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, vol. 10, no. 12, 1990, pp. 3873-9.
Courtney MJ, Lambert JJ, Nicholls DG. The interactions between plasma membrane depolarization and glutamate receptor activation in the regulation of cytoplasmic free calcium in cultured cerebellar granule cells. J Neurosci. 1990;10(12):3873-9.
Courtney, M. J., Lambert, J. J., & Nicholls, D. G. (1990). The interactions between plasma membrane depolarization and glutamate receptor activation in the regulation of cytoplasmic free calcium in cultured cerebellar granule cells. The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 10(12), 3873-9.
Courtney MJ, Lambert JJ, Nicholls DG. The Interactions Between Plasma Membrane Depolarization and Glutamate Receptor Activation in the Regulation of Cytoplasmic Free Calcium in Cultured Cerebellar Granule Cells. J Neurosci. 1990;10(12):3873-9. PubMed PMID: 1980131.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The interactions between plasma membrane depolarization and glutamate receptor activation in the regulation of cytoplasmic free calcium in cultured cerebellar granule cells. AU - Courtney,M J, AU - Lambert,J J, AU - Nicholls,D G, PY - 1990/12/1/pubmed PY - 1990/12/1/medline PY - 1990/12/1/entrez SP - 3873 EP - 9 JF - The Journal of neuroscience : the official journal of the Society for Neuroscience JO - J Neurosci VL - 10 IS - 12 N2 - The complex modulation of cytoplasmic free calcium concentration ([Ca2+]c) in primary cultures of cerebellar granule cells in response to glutamate receptor agonists has been the subject of several contradictory reports. We here show that 3 components of the [Ca2+]c response can be distinguished: (1) Ca2+ entry through voltage-dependent Ca2+ channels, following KCl- or receptor-evoked depolarization, (2) Ca2+ entry through NMDA receptor channels, and (3) liberation of internal Ca2+ via a metabolotropic receptor. Depolarization with KCl induced a transient [Ca2+]c response (subject to voltage inactivation) decaying to a sustained plateau (largely inhibited by nifedipine). The NMDA response was potentiated by glycine, totally inhibited by (+)5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801), and blocked by Mg2+ in a voltage-sensitive manner. Polarized cells displayed small responses to quisqualate (QA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA). Depolarization enhanced a transient response to QA, but not to AMPA. Trans-1-amino-1,3-cyclopentanedicarboxylic acid (trans-ACPD), a selective agonist for the metabolotropic glutamate receptor, caused a transient elevation of [Ca2+]c, which was blocked by prior exposure to QA but not AMPA. The prolonged [Ca2+]c response to kainate (KA) can be resolved into 2 major components: an indirect NMDA receptor-mediated response due to released glutamate and a nifedipine-sensitive component consistent with depolarization-mediated entry via Ca2+ channels. 6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX), QA at greater than 10 microM, and AMPA (but not trans-ACPD) reversed the KA response, consistent with an inactivation of the KA receptor.(ABSTRACT TRUNCATED AT 250 WORDS) SN - 0270-6474 UR - https://www.unboundmedicine.com/medline/citation/1980131/The_interactions_between_plasma_membrane_depolarization_and_glutamate_receptor_activation_in_the_regulation_of_cytoplasmic_free_calcium_in_cultured_cerebellar_granule_cells_ L2 - http://www.jneurosci.org/cgi/pmidlookup?view=long&pmid=1980131 DB - PRIME DP - Unbound Medicine ER -