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2. Interleukin-1 enhances the ATP-evoked release of arachidonic acid from mouse astrocytes.

Author

Stella, N, Estellés, A, Siciliano, J, Tencé, M, Desagher, S, Piomelli, D, Glowinski, J, and Prémont, J

Subjects
Astrocytes, Animals, Mice, Arachidonic Acids, Adenosine Triphosphate, Interleukin-1, Dose-Response Relationship, Drug, purinoceptor, phospholipase, cytokine, inflammation, glutamate, neurotoxicity, Dose-Response Relationship, Drug, Neurology & Neurosurgery, Medical and Health Sciences, Psychology and Cognitive Sciences
Abstract

During neuropathological states associated with inflammation, the levels of cytokines such as interleukin-1beta (IL-1beta) are increased. Several studies have suggested that the neuronal damage observed in pathogenesis implicating IL-1beta are caused by an alteration in the neurochemical interactions between neurons and astrocytes. We report here that treating striatal astrocytes in primary culture with IL-1beta for 22-24 hr enhances the ATP-evoked release of arachidonic acid (AA) with no effect on the ATP-induced accumulation of inositol phosphates. The molecular mechanism responsible for this effect involves the expression of P2Y2 receptors (a subtype of purinoceptor activated by ATP) and cytosolic phospholipase A2 (cPLA2, an enzyme that mediates AA release). Indeed, P2Y2 antisense oligonucleotides reduce the ATP-evoked release of AA only from IL-1beta-treated astrocytes. Further, both the amount of cPLA2 (as assessed by Western blotting) and the release of AA resulting from direct activation of cPLA2 increased fourfold in cells treated with IL-1beta. We also report evidence indicating that the coupling of newly expressed P2Y2 receptors to cPLA2 is dependent on PKC activity. These results suggest that during inflammatory conditions, IL-1beta reveals a functional P2Y2 signaling pathway in astrocytes that results in a dramatic increase in the levels of free AA. This pathway may thus contribute to the neuronal loss associated with cerebral ischemia or traumatic brain injury.

Published
1997

3. Inhibition by anandamide of gap junctions and intercellular calcium signalling in striatal astrocytes.

Author

Venance, L, Piomelli, D, Glowinski, J, and Giaume, C

Subjects
Corpus Striatum, Astrocytes, Cells, Cultured, Gap Junctions, Animals, Mice, Rats, Calcium, Cyclohexanols, Cannabinoids, Benzoxazines, Morpholines, Isoquinolines, Naphthalenes, Arachidonic Acids, Glutamic Acid, Endocannabinoids, Signal Transduction, Cell Membrane Permeability, Polyunsaturated Alkamides, Cells, Cultured, General Science & Technology
Abstract

Anandamide, an endogenous arachidonic acid derivative that is released from neurons and activates cannabinoid receptors, may act as a transcellular cannabimimetic messenger in the central nervous system. The biological actions of anandamide and the identity of its target cells are, however, still poorly documented. Here we show that anandamide is a potent inhibitor of gap-junction conductance and dye permeability in striatal astrocytes. This inhibitory effect is specific for anandamide as compared to co-released congeners or structural analogues, is sensitive to pertussis toxin and to protein-alkylating agents, and is neither mimicked by cannabinoid-receptor agonists nor prevented by a cannabinoid-receptor antagonist. Glutamate released from neurons evokes calcium waves in astrocytes that propagate via gap junctions, and may, in turn, activate neurons distant from their initiation sites in astrocytes. We find that anandamide blocks the propagation of astrocyte calcium waves generated by either mechanical stimulation or local glutamate application. Thus, by regulating gap-junction permeability, anandamide may control intercellular communication in astrocytes and therefore neuron-glial interactions.

Published
1995

25. Sequential and opposite regulation of two outward [K.sup.+] currents by ET-1 in cultured striatal astrocytes

Author

BYCHKOV, R., GLOWINSKI, J., and GIAUME, C.

Subjects
Cellular control mechanisms -- Research, Cytochemistry -- Research, Astrocytes -- Physiological aspects, Brain research -- Research, Potassium -- Physiological aspects, Neuroglia -- Physiological aspects, Homeostasis -- Physiological aspects, Cells -- Permeability, Biological sciences
Abstract

In the brain, astrocytes represent a major target for endothelins (ETs), a family of peptides that can be released by several cell types and that have potent and multiple effects on astrocytic functions. Four types of [K.sup.+] currents ([I.sub.K]) were detected in various proportions by patch-clamp recordings of cultured striatal astrocytes, including the A-type [I.sub.K], the inwardly rectifying [I.sub.K IR], the [Ca.sup.2+]-dependent [I.sub.K] ([I.sub.K Ca]), and the delayed-rectified [I.sub.K] ([I.sub.K DR]). Variations in the shape of current-voltage relationships were related mainly to differences in the proportion of these currents. ET-1 was found to regulate with opposite effects the two more frequently recorded outward [K.sup.+] currents in striatal astrocytes. Indeed, this peptide induced an initial activation Of [I.sub.K Ca] (composed of SK and BK channels) and a delayed long-lasting inhibition of [I.sub.K DR]. In current-clamp recordings, the activation of [I.sub.K Ca] correlated with a transient hyperpolarization, whereas the inhibition of [I.sub.K DR] DR correlated with a sustained depolarization. These ET-1-induced sequential changes in membrane potential in astrocytes may be important for the regulation of voltage gradients in astrocytic networks and the maintenance of [K.sup.+] homeostasis in the brain microenvironment. glial cells; endothelins; calcium-dependent potassium channels

Published
2001

44. Abstracts

Author

Abdullah, Lubna H., Buchanan, K. D., Akopyan, T. N., Arzumanyan, A. M., Arutunyan, A. A., Berger, H., Oehme, P., Atkinson, M. E., Chaggar, J. S., Bailey, S. J., Featherstone, R. L., Jordan, C. C., Morton, I. K. M., Balfe, A., Skrabanek, P., Powell, D., Barja, F., Mathison, R., Huggel, H., Bittiger, H., Heid, J., Björkroth, Ulla, Rosell, Sune, Boyd, N. D., Anthony, M. P., Leeman, S. E., Briggs, I., Growcott, J. W., Jamieson, A., Tarpey, Ann V., Brodin, E., Meyerson, B. A., Brown, J. R., Hayes, A. G., Meecham, K. G., Tyers, M. B., Burcher, E., Bynke, G., Håkanson, R., Hörig, J., Cann, John R., Rahim, Iffat, Vatter, Albert, Stewart, John M., Cascieri, Margaret A., Liang, Tehming, Cheeseman, H. J., Pinnock, R. O., Henderson, G., Constantinidis, J., Bouras, C., Taban, C. H., Guntern, R., Couture, R., Cuello, A. C., Dalsgaard, C. -J., Jonsson, C. -E., Arvidsson, J., Risling, M., Hökfelt, T., Schultzberg, M., Vincent, S. R., Elfvin, L. -G., de Beaurepaire, R., Iversen, S. D., Delbro, D., Lisander, B., Fändriks, L., Andersson, S. A., Del Fiacco, M., Dessi, M. L., Levarvti, M. C., Del Rio, J., Naranjo, J. R., Domschke, S., Bloom, S. R., Adrian, T. E., Lux, G., Bryant, M. G., McGregor, G. P., Domschke, W., Donnerer, J., Barthó, L., Holzer, P., Lembeck, F., Skofitsch, G., Elliott, P. J., Bannon, M. J., Alpert, J. E., Ferri, G. -L, McGregor, G., Vezzadini, P., Labo, G., Polak, J. M., Fontaine-Perus, J. C., Chanconie, M., Foreman, J. C., Piotrowski, W., Fox, J. E. T., Daniel, E. E., Jury, J., Domoto, T., Berezin, I., Gaudino, G., Mondardini, L., Fasolo, A., Gazelius, B., Kahan, T., Panopoulos, P., Olgart, L., Gintzler, Alan R., Jaffe, Bernard M., Baron, Sheri A., GrÖnstad, K. O., Ahlman, H., Zinner, M. J., Jaffe, B. M., Yeo, C., Gu, J., Huang, W. M., lslam, K. N., Terenghi, G., Morrison, J., Güllner, H. -G., Haeusler, Guenther, Handelmann, Gail E., Selsky, Joyce H., Helme, R. D., White, D. M., Höfler, H., Heitzt, Ph. U., Auböck, L., Petsche, Ulrike, Lippe, Irmgard, Hylden, Janice L. K., Wilcox, George L., Inoue, Atsuko, Nakata, Yoshihiro, Segawa, Tomio, Jakubowska-Naziemblo, B., Potargowicz, E., Traczyk, W. Z., Cannon, D., Rohde, W., JancsÓ, G., Király, E., Karcsú, S., Szebeni, A., Bácsy, E., Jones, R. S. G., Olpe, H. -R., Wrightt, D. M., Jurna, I., Kerdelhué, B., Lenoir, V., Pasqualini, C., El Abed, A., Morel, G., Dubois, P., Hublot, P., Tartar, A., Klingmúller, D., Waltz, C., Kramer, H. J., Koop, H., Luster, W., Gropp, C., Havemenn, K., Arnold, R., Krause, James E., McKelvy, Jeffrey F., Krivoy, W., Couch, J., Strand, F., Leander, S., Folkers, K., Lee, C. M., Snyder, S. H., Lindberg, P., Dahlström, A., Lundberg, J. M., Lindefors, N., Ungerstedt, U., Liu-Chen, L. -Y., Liszczak, T., Mayberg, M. R., Moskowitz, M. A., Lundberg, Jan M., Saria, Alois, Brodin, Ernst, Martling, Claes-Roland, Hökfelt, Tomas, Lundblad, Lars, Änggård, Anders, McGeeney, K. F., O'Donnell, M. D., Blank, M. A., Manolas, K., Linger, W. G., Allen, J. M., Maggio, J. E., Sandberg, B. E. B., Bradley, C. V., Iversen, L. L., Santikarn, S., Williams, D. H., Hunter, J. C., Hanley, M. R., Magnusson, I., Thulin, L., Mandahl, Agneta, Bill, Anders, Manning, Maurice, Martensson, H., Akande, B., Stofer, P., Chappuis, G., Immer, H., Groog, P., Matthews, Margaret R., Connaughton, M., Moratalla, R., Nobin, Anders, Emson, Piers, Sundler, Frank, O'Donohue, T. L., Shults, C. W., Quirion, R., Moody, T. W., Chase, T. N., Otsuka, M., Konishi, S., Yanagisawa, M., Akagi, H., Otten, U., Rüegg, U. T., Pawlik, W., Konturek, S. J., Kania, J., Gustaw, P., Cosgrove, Patricia G., Pazoles, Christopher J., Priestley, J. V., Jensen, R. T., Pert, C. B., Regoli, D., Mizrahi, J., D'Orléans-Juste, P., Caranikas, S., Escher, E., Folkers, Karl, Rüegg, Urs T., Bishai, W. R., Saria, A., Rama Sastry, B. V., Jaiswal, Neelam, Tayeb, Osama S., Schultheiss, Hartmut, Hörig, Joachim, Scott, T. M., Shanahan, F., Befus, A. D., Fox, J., Denburg, J. A., Bienenstock, J., Sheppard, M. N., Kurian, S. S., Siegel, R. A., Weidenfeld, J., Globus, M., Melamed, E., Sjödin, L., Srivastava, G., Hall, Michael E., Suhar, A., Turk, V., Marks, N., Szkudlarek, U., Tarkkanen, A., Tervo, T., Tervo, K., Eränkö, L., Eränkö, O., Huang, W. -M., Morrison, J. F. B., Unger, W. G., Tessler, A., Himes, B. T., Murray, M., Goldberger, M. E., Torrens, Y., Beaujouan, J. C., Viger, A., Glowinski, J., Casanueva, F. F., Knuth, E., Havlicek, V., Friesen, H. G., Triepel, J., Weindl, A., Reinecke, M., Mader, J., Forssmann, W. G., Unger, Thomas, Becker, Hans, König, Manfred, Ganten, Detlev, Lang, Rudolf E., Vacca, L. L., Naftchi, N. E., Guan, X. -M., Ai, M. -K., Vijayan, E., Wang, Y. M., Mashford, M. L., Watson, Stephen P., Sandberg, Bengt E. B., Iversen, Leslie L., Weihe, E., Hartschuh, W., Kuchling, G., Winter, E. A., Keen, P., Yeo, C. J., Ylikoski, Jukka, Tervo, Timo, Tervo, Kaarina, Eränko, Liisa, and Cuello, Claudio

Published
1983
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49. Mechanism of the oxidation of nitric oxide with oxygen

Author

Głowiński Józef, Józef Hoffmann, and Wilk Marcin

Subjects
nitrogen monoxide, oxygen, mechanism, kinetic, equilibrium, nitrogen trioxide, Chemistry, QD1-999
Abstract

Very fast reactions of forming higher nitrogen oxides set out an equilibrium framework for the course of the reaction of nitrogen monoxide oxidation. The slow course of reaction of nitrogen monoxide with oxygen permanently violates the created equilibria. In particular, the equilibrium of the oxidation reaction of nitrogen monoxide with nitrogen dioxide. The contribution of this reaction to the transformation of nitrogen monoxide in the conditions of nitrogen trioxide removal from the gas phase was estimated.

Published
2021
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