The time course of NMDA-and kainate-induced cGMP elevation and glutamate release in cultured neuron

Archives of Pharmacal Research - Tập 18 - Trang 153-158 - 1995
Seikwan Oh1, Chang Sik Shin2, Hack Seang Kim2
1Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, USA
2Department of Pharmacology, College of Pharmacy, Chungbuk National University, Cheongiu, Korea

Tóm tắt

The levels of extracellular glutamate, intracellular Ca2+ ([Ca2+]i) and cGMP were determined for 1 h with the excitatory amino acids, N-methyl-D-aspartate (NMDA) or kainate in cultured cerebellar granule cells. Both NMDA and kainate produced a time-dependent release of glutamate, and kainate was more potent than NMDA in glutamate elevation. The elevation of extracellular glutamate was not purely governed by intracellular Ca2+ concentration. However, in opposite to the time-dependent elevation of glutamate, the elevation of cGMP by NMDA and kainate were at maximum level in short-time (1 min) incubation then remarkably decreased with longer incubation times. Post-applications (30 min after agonist) of EAA antagonst did not block EAAs-induced glutamate elevation. However, NMDA antagonist, phencyclidine (PCP), blocked NMDA-induced cGMP elevation at pre- or post-application, but kainate antagonist, 6,7-dinitroquinoxaline-2,3-dione (DNQX), paradoxically augmented kainate-induced cGMP elevation for 1 h incubation. These results show that NMDA or kainate induces time-dependent elevations of extracellular glutamate, while the elevations of cGMP by these EAAs are remarkably decreased with longer incubation times. However, NMDA- and kainate-induced glutamate release was blocked by pre-application of each receptor antagonist but not by post-application while EAA-induced [Ca2+]i was blocked by post-application of antagonist. These observations suggest that EAA-induced elevation of [Ca2+]i is not parallel with elevation of glutamate release or cGMP.

Tài liệu tham khảo

Adam-Vizi, V., External Ca2+-dependent release of neurotransmitters.J. Neurochem., 58, 395–405 (1992). Attwell, D., Barbour, B. and Szatkowski, M., Nonvesicular release of neurotransmitter.Neuron, 11, 401–407 (1993). Bliss, T. V. and Collingridge, G. L., A synaptic model of memory: long-term potentiation in the hippocampus.Nature, 361, 31–39 (1993). Bourne, H. R. and Nicoll, R., Molecular machines integrate coincident synaptic signals.Cell/Neuron. 72/10 (supple.) 65–75 (1993). Bouvier, M., Szatkowski, M., Amato, A. and Attwell, D., The glial cell glutamate uptake carrier counter-transports pH-changing anions.Nature, 360, 471–474 (1992). Bradford, M. M., A rapid sensitive method for the quantitation of microgram quantities of protein utilizing the principle of Protein-dye binding.Analyt. Biochem., 72, 248–254 (1976). Bredt, D. S. and Snyder, S. H., Nitric oxide mediates glutamate-linked enhancement of cGMP levels in the cerebellum.Proc. Natl. Acad. Sci. USA, 86, 9030–9033 (1989). Brew, H. and Attwell, D., Electrogenic glutamate uptake is a major current carrier in the membrane of axonal retinal glial cells.Nature, 327, 707–709 (1987). Brewer, G. J. and Cotman, C. W., NMDA receptor regulation of neuronal morphology in cultured hippocampal neurons.Neurosci. Lett., 99, 268–273 (1989). Cai, Z. and McCaslin, P. P., Amitriptyline, desipramine, cyproheptadine and carbamazepine, in concentrations used therapeutically, reduced kainate-and N-methyl-D-aspartate-induced intracellular Ca2+ levels in neuronal culture.Eur. J. Pharmacol., 219, 53–57 (1992). Choi, D. W., Maulucci-Gedde, M. and Kriegstein, A. R., Glutamate neurotoxicity in cortical cell culture.J. Neurosci. 7, 357–368 (1987). Collingridge, G. L. and Bliss, T. V. P., NMDA receptors-their role in long term potentiation.Trends Neurosci., 10, 288–293 (1987). Collingridge, G. L. and Lester, R. A. J., Excitatory amino acid receptors in the vertebrate central nervous system.Pharmacol. Rev., 40, 143–210 (1989). Cull-Candy, S. G. and Usowicz, M. M., Multiple-con-ductance channels activated by excitatory amino acids in cerebellar neurons.Nature, 325, 525–528 (1987). De Camilli, P. and Jahn, R., Pathways to regulated exocytosis in neurons.Ann. Rev. Physiol., 52, 625–645 (1990). Ellison, D. W., Beal, M. F. and Martin, J. B., Amino acid neurotransmitters in postmortem human brain analyzed by high performance liquid chromatography with electrochemical detection.J. Neurosci. Metho., 19 305–315 (1987). Flot, B. and Seifert, W., Characterization of glutamate uptake systems in astrocyte primary cultures from rat brain.Glia, 4, 293–304 (1991). Garthwaite, J., Charles, S. L. and Chess-Williams, R., Endothelium-derived relaxing factor release on activation of NMDA receptors suggests role as inter-cellular messenger in the brain.Nature, 336, 385–388 (1988). Gathwaite, J., Excitatory amino acid receptors and guanosine 3′,5′-cyclic monophosphate in incubated slices of immature and adult rat cerebellum.Neuroscience, 7, 2491–2497 (1982). Grynkiewicz, G., Poenie, M. and Tsien, R. Y., A new generation of Ca2+ indicators with greatly improved fluorescence properties.J. Biol. Chem. 260, 3440–3450 (1985). Harper, J. F. and Brooker, G., Femtomole sensitive radioimmunoassay for cyclic AMP and cyclic GMP after 2′O acetylation by acetic anhydride in aqueous solution.J. Cyclic. Nucleotide Res., 1, 207–218 (1975). Jahr, C. E., Stevens, C. F., Glutamate activates multiple single channel conductances in hippocampal neurones.Nature, 325, 522–525 (1987). Jessell, A. M. and Kandel, E. R., Synaptic transmission: a bidirectional and self-modifiable form of cell-cell communication.Cell 72/Neuron 10 (Suppl.), 1–30 (1993). Kostyuk, P. G. and Tepikin, A. V., Calcium signals in nerve cells.News Physiol. Sci., 6, 6–10 (1991). Mayer, M. L. and Westbrook, G. L., The physiology of excitatory amino acids in the vertebrate central nervous system.Prog. Neurobiol., 28, 197–276 (1987). McCaslin, P. P. and Morgan, W. W., Cultured cerebellar cells as an in vitro model of excitatory amino acid receptor function.Brain Res., 417, 380–384 (1987). Monaghan, D. T., Bridges, S. R. and Cotman, C. W., The excitatory amino acid receptors: Their classes, pharmacology, and distinct properties in the function of the central nervous system.Ann. Rev. Pharm. Toxi., 29, 365–402 (1989). Morgan, J. I. and Curran, T., Role of ion flux in the control of c-fos expression.Nature. 322, 552–555 (1986). Rosenmund, C. and Westbrook, G. L., Calcium-indcued actin depolymerization reduces NMDA channel activity.Neuron, 10, 805–814 (1993). Schoepp, D. D., Bockaert, J. and Sladeczek, F., Pharmacological and functional characteristics of metabotropic excitatory amino acid receptors.Trends Pharmacol. Sci, 11, 508–515 (1990). Vincent, S. R. and Hope, B. T., Neurons that say NO.Trends Neurosci, 15, 108–113 (1992).