Perinatal Hypoxic-Ischemic Brain Injury Enhances Quisqualic Acid-Stimulated Phosphoinositide Turnover
dc.contributor.author | Chen, Chu-Kuang | en_US |
dc.contributor.author | Silverstein, Faye Sarah | en_US |
dc.contributor.author | Fisher, Stephen K. | en_US |
dc.contributor.author | Statman, Daniel | en_US |
dc.contributor.author | Johnston, Michael V. | en_US |
dc.date.accessioned | 2010-04-01T15:32:01Z | |
dc.date.available | 2010-04-01T15:32:01Z | |
dc.date.issued | 1988-08 | en_US |
dc.identifier.citation | Chen, Chu-Kuang; Silverstein, Faye S.; Fisher, Stephen K.; Statman, Daniel; Johnston, Michael V. (1988). "Perinatal Hypoxic-Ischemic Brain Injury Enhances Quisqualic Acid-Stimulated Phosphoinositide Turnover." Journal of Neurochemistry 51(2): 353-359. <http://hdl.handle.net/2027.42/66017> | en_US |
dc.identifier.issn | 0022-3042 | en_US |
dc.identifier.issn | 1471-4159 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/66017 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=2839619&dopt=citation | en_US |
dc.description.abstract | In an experimental model of perinatal hypoxic-ischemic brain injury, we examined quisqualic acid (Quis)-stimulated phosphoinositide (PPI) turnover in hippocampus and striatum. To produce a unilateral forebrain lesion in 7-day-old rat pups, the right carotid artery was ligated and animals were then exposed to moderate hypoxia (8% oxygen) for 2.5 h. Pups were killed 24 h later and Quis-stimulated PPI turnover was assayed in tissue slices obtained from hippocampus and striatum, target regions for hypoxic-ischemic injury. The glutamate agonist Quis (10 -4 M ) preferentially stimulated PPI hydrolysis in injured brain. In hippocampal slices of tissue derived from the right cerebral hemisphere, the addition of Quis stimulated accumulation of inositol phosphates by more than ninefold (1,053 ± 237% of basal, mean ± SEM, n = 9). In contrast, the addition of Quis stimulated accumulation of inositol phosphates by about fivefold in the contralateral hemisphere (588 ± 134%) and by about sixfold in controls (631 ± 177%, p < 0.005, comparison of ischemic tissue with control). In striatal tissue, the corresponding values were 801 ± 157%, 474 ± 89%, and 506 ± 115% (p < 0.05). In contrast, stimulation of PPI turnover elicited by the cho-linergic agonist carbamoylcholine, (10 -4 or 10 -2 M ) was unaffected by hypoxia-ischemia. The results suggest that prior exposure to hypoxia-ischemia enhances coupling of excitatory amino acid receptors to phospholipase C activity. This activation may contribute to the pathogenesis of irreversible brain injury and/or to mechanisms of recovery. | en_US |
dc.format.extent | 783497 bytes | |
dc.format.extent | 3110 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | Blackwell Publishing Ltd | en_US |
dc.rights | 1988 International Society for Neurochemistry Ltd. | en_US |
dc.subject.other | Quisqualic Acid | en_US |
dc.subject.other | Inositol Phospholipids | en_US |
dc.subject.other | Hippocampus | en_US |
dc.subject.other | Striatum | en_US |
dc.subject.other | Carbamoylcholine | en_US |
dc.subject.other | Perinatal | en_US |
dc.subject.other | Hypoxia-ischemia | en_US |
dc.title | Perinatal Hypoxic-Ischemic Brain Injury Enhances Quisqualic Acid-Stimulated Phosphoinositide Turnover | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Neurosciences | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Pharmacology, University of Michigan Medical School | en_US |
dc.contributor.affiliationum | Center for Human Growth and Development, University of Michigan, Ann Arbor, Michigan, U.S.A. | en_US |
dc.contributor.affiliationother | * Neuroscience Program | en_US |
dc.contributor.affiliationother | Department of Pediatrics and Neurology | en_US |
dc.identifier.pmid | 2839619 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/66017/1/j.1471-4159.1988.tb01046.x.pdf | |
dc.identifier.doi | 10.1111/j.1471-4159.1988.tb01046.x | en_US |
dc.identifier.source | Journal of Neurochemistry | en_US |
dc.identifier.citedreference | Abe K., Kogure K., Yamamoto H., Imazawa M., and Miyamoto K. ( 1987 ) Mechanism of arachidonic acid liberation during ischemia in gerbil cerebral cortex. J. Neurochem. 48, 503 – 509. | en_US |
dc.identifier.citedreference | Bazan N. ( 1970 ) Effects of ischemia and electroconvulsive shock on free fatty acid pool in the brain. Biochim. Biophys. Acta 218, 1 – 10. | en_US |
dc.identifier.citedreference | Berridge M. J. ( 1984 ) Inositol triphosphate and diacylglycerol as second messengers. Biochem. J. 220, 345 – 360. | en_US |
dc.identifier.citedreference | Berridge M. J. and Irvine R. F. ( 1984 ) Inositol triphosphate, a novel second messenger in cellular signal transduction. Nature 312, 315 – 321. | en_US |
dc.identifier.citedreference | Berridge M. J., Downes P. C., and Hanley M. R. ( 1982 ) Lithium amplifies agonist dependent phosphatidyl inositol response in brain and salivary gland. Biochem. J. 206, 587 – 595. | en_US |
dc.identifier.citedreference | Berridge M. J., Dawson R. M. C., Downes C. P., Heslop J. P., and Irvine R. F. ( 1983 ) Changes in the levels of inositol phosphates after agonist-dependent hydrolysis of membrane phosphoino-sitides. Biochem. J. 212, 473 – 482. | en_US |
dc.identifier.citedreference | Chen C.-K., Silverstein F. S., Fisher S. K., Statman D., and Johnston M. V. ( 1987 ) Perinatal hypoxia-ischemia enhances quisqualic acid stimulated phosphoinositide turnover. Soc. Neur-osci. Abstr. 13, 755. | en_US |
dc.identifier.citedreference | Choi D. W., Maulucci-Gedde M., and Kriegstein A. R. ( 1987 ) Glutamate neurotoxicity in cortical cell culture. J. Neurosci. 357 – 368. | en_US |
dc.identifier.citedreference | Eva C. and Costa E. ( 1986 ) Potassium ion facilitation of phosphoinositide turnover activation by muscarinic receptor agonists in rat brain. J. Neurochem. 46, 1429 – 1435. | en_US |
dc.identifier.citedreference | Fisher S. K. and Agranoff B. W. ( 1987 ) Receptor activation and inositol lipid hydrolysis in neural tissues. J. Neurochem. 48, 999 – 1017. | en_US |
dc.identifier.citedreference | Fisher S. K. and Bartus R. T. ( 1985 ) Regional differences in the coupling of muscarinic receptors to inositol phospholipid hydrolysis in guinea pig brain. J. Neurochem. 45, 1085 – 1095. | en_US |
dc.identifier.citedreference | Fisher S. K., Figueiredo J. C., and Bartus R. T. ( 1984 ) Differential stimulation of inositol phospholipid turnover in brain by analogs of oxotremorine. J. Neurochem. 43, 1171 – 1179. | en_US |
dc.identifier.citedreference | Greenamyre J. T., Penney J. B., Young A. B., Hudson C., Silver-stein F. S., and Johnston M. V. ( 1987 ) Evidence for transient perinatal glutamatergic innervation of globus pallidum. J. Neurosci. 1022 – 1030. | en_US |
dc.identifier.citedreference | Heacock A.M., Fisher S. K., and Agranoff B. W. ( 1987 ) Enhanced coupling of neonatal muscarinic receptors in rat brain to phosphoinositide turnover. J. Neurochem. 48, 1904 – 1911. | en_US |
dc.identifier.citedreference | Iadarola M. J., Nicoletti F., Naranjo J. R., Putnam F., and Costa E. ( 1986 ) Kindling enhances the stimulation of inositol phospholipid hydrolysis elicited by ibotenic acid in rat hippocampal slices. Brain Res : 374, 174 – 178. | en_US |
dc.identifier.citedreference | Ikeda M., Yoshida S., Busto R., Santiso M., and Ginsberg M. D. ( 1986 ) Polyphosphoinositides as a probable source of brain free fatty acids accumulated at the onset of ischemia. J. Neurochem. 47, 123 – 132. | en_US |
dc.identifier.citedreference | Johnston M. V. ( 1983 ) Neurotransmitter alterations in a model of perinatal hypoxic-ischemic brain injury. Ann. Neurol. 16, 511 – 518. | en_US |
dc.identifier.citedreference | Jorgensen M. D. and Diemer N. A. ( 1982 ) Selective neuron loss after cerebral ischemia in the rat: possible role of transmitter glutamate. Acta Neurol. Scand. 66, 536 – 546. | en_US |
dc.identifier.citedreference | Kirino T. ( 1981 ) Delayed neuronal death in the gerbil hippocampus following ischemia. Brain Res. 239, 57 – 69. | en_US |
dc.identifier.citedreference | Lowry O. H., Rosebrough N. J., Farr A. L., and Randall R. J. ( 1951 ) Protein measurements with the Folin phenol reagent. J. Biol. Chem. 193, 265 – 275. | en_US |
dc.identifier.citedreference | Meldrum B. ( 1985 ) Excitatory amino acids and anoxic-ischemic brain damage. Trends Neurosci. 47 – 48. | en_US |
dc.identifier.citedreference | Nicoletti F., Iadorola M. J., Wroblewski J. T., and Costa E. ( 1986a ) Coupling of inositol phospholipid metabolism with excitatory amino acid recognition sites in rat hippocampus. J. Neurochem. 46, 40 – 46. | en_US |
dc.identifier.citedreference | Nicoletti F., Iadarola M. J., Wroblewski J. T., and Costa E. ( 1986b ) Excitatory amino acid recognition sites coupled with inositol phospholipid metabolism: developmental changes and interaction with alpha 1 -adrenoreceptors. Proc. Natl. Acad. Sci. USA 83, 1931 – 1935. | en_US |
dc.identifier.citedreference | Nishizuka Y. ( 1986 ) Turnover of inositol phospholipids and signal transduction. Science 233, 305 – 312. | en_US |
dc.identifier.citedreference | Pearce B., Albrecht B., Morrow C., and Murphy S. ( 1986a ) Astro-cyte glutamate receptor activation promotes inositol phospholipid turnover and calcium flux. Neurosci. Leu. 72, 335 – 340. | en_US |
dc.identifier.citedreference | Pearce B., Morrow C., and Murphy S. ( 1986b ) Receptor mediated inositol phospholipid hydrolysis in astrocytes. Eur. J. Pharmacol. 121, 231 – 243. | en_US |
dc.identifier.citedreference | Raichle M. ( 1983 ) The pathophysiology of brain ischemia. Ann. Neurol. 13, 2 – 10. | en_US |
dc.identifier.citedreference | Rothman S. and Olney J. ( 1986 ) Glutamate and the pathophysiology of hypoxic-ischemic brain damage. Ann. Neurol. 19, 105 – 111. | en_US |
dc.identifier.citedreference | Silverstein F. S., Chen R. C., and Johnston M. V. ( 1986 ) The glutamate agonist quisqualic acid is neurotoxic in striatum and hippocampus of immature rat brain. Neurosci Lett. 71, 13 – 18. | en_US |
dc.identifier.citedreference | Silverstein F. S., Torke L., Barks J., and Johnston M. V. ( 1987 ) Hypoxia-ischemia produces focal disruption of glutamate receptors in developing brain. Dev. Brain Res. 34, 33 – 39. | en_US |
dc.identifier.citedreference | Simon R. P., Griffiths T., Evans M. C., Swan J. H., and Meldrum B. S. ( 1984 ) Calcium overload in selectively vulnerable neurons of the hippocampus during and after ischemia: an electron microscopy study in the rat. J. Cereb. Blood Flow Metab. 4, 350 – 361. | en_US |
dc.identifier.citedreference | Sladeczek F., Pin J. P., Recasens M., Bockart J., and Weiss S. ( 1985 ) Glutamate stimulates inositol phosphate formation in striatal neurons. Nature 311, 717 – 719. | en_US |
dc.identifier.citedreference | Westerberg E. and Wieloch T. ( 1986 ) Lesions to the corticostriatal pathways ameliorate hypoglycemia-induced arachidonic acid release. J. Neurochem. 47, 1507 – 1511. | en_US |
dc.identifier.citedreference | Yoshida S., Ikeda M., Busto R., Santiso M., Martinez E., and Ginsberg M. ( 1986 ) Cerebral phosphoinositide, triacylglyc-erol, and energy metabolism in reversible ischemia: origin and fate of free fatty acids. J. Neurochem. 47, 744 – 757. | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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