Excitotoxic Brain Injury Suppresses Striatal High-Affinity Glutamate Uptake in Perinatal Rats
dc.contributor.author | Hu, Bernadine | en_US |
dc.contributor.author | McDonald, John W. | en_US |
dc.contributor.author | Johnston, Michael V. | en_US |
dc.contributor.author | Silverstein, Faye Sarah | en_US |
dc.date.accessioned | 2010-04-01T15:05:32Z | |
dc.date.available | 2010-04-01T15:05:32Z | |
dc.date.issued | 1991-03 | en_US |
dc.identifier.citation | Hu, Bernadine; McDonald, John W.; Johnston, Michael V.; Silverstein, Faye S. (1991). "Excitotoxic Brain Injury Suppresses Striatal High-Affinity Glutamate Uptake in Perinatal Rats." Journal of Neurochemistry 56(3): 933-937. <http://hdl.handle.net/2027.42/65556> | en_US |
dc.identifier.issn | 0022-3042 | en_US |
dc.identifier.issn | 1471-4159 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/65556 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=1671587&dopt=citation | en_US |
dc.description.abstract | In immature rodent brain, the glutamate receptor agonist N -methyl-D-aspartate (NMDA) is a potent neurotoxin. In postnatal day (PND)-7 rats, intrastriatal injection of 25 nmol of NMDA results in extensive ipsilateral forebrain injury. In this study, we examined alterations in high-affinity [ 3 H]glutamate uptake (HAGU) in NMDA-lesioned striatum. HAGU was assayed in synaptosomes, prepared from lesioned striatum, the corresponding contralateral striatum, or unlesioned controls. Twenty-four hours after NMDA injection (25 nmol), HAGU declined 44 ± 8% in lesioned tissue, compared with the contralateral striatum (mean ± SEM, n = 6 assays, p < 0.006, paired t test). Doses of 5–25 nmol of NMDA resulted in increasing suppression of HAGU (5 nmol, n = 3; 12.5 nmol, n = 3; and 25 nmol, n = 5 assays; p < 0.01, regression analysis). The temporal evolution of HAGU suppression was biphasic. There was an early transient suppression of HAGU (−28 ± 4% at 1 h; p < 0.03, analysis of variance, comparing changes at 0.5, 1, 2, and 3 h after lesioning); 1 or 5 days postinjury there was sustained loss of HAGU (at 5 days, −56 ± 11%, n = 3, p < 0.03, paired t test, lesioned versus contralateral striata). Treatment with the noncompetitive NMDA antagonist MK-801 (1 mg/kg i.p.) attenuated both the early and subsequent irreversible suppression of HAGU (1 h postlesion −28 ± 4%, n = 6 assays versus −12.6 ± 5% with MK-801, n = 4, p = 0.005; 24 h postlesion, −44 ± 8%, n = 5, versus +2.4 ± 6%, n = 3 with MK-801, p = 0.01, Wilcoxon ranked sum tests). In immature brain excitotoxic lesions produce an acute reversible suppression of HAGU, and a delayed long-lasting reduction in HAGU secondary to brain injury. These data suggest that accumulation of endogenous glutamate, as a consequence of the acute disruption of HAGU, could contribute to the pathogenesis of excitotoxic neuronal injury. | en_US |
dc.format.extent | 585436 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 | 1991 International Society for Neurochemistry Ltd. | en_US |
dc.subject.other | Perinatal | en_US |
dc.subject.other | N -Methyl-D-Aspartate | en_US |
dc.subject.other | Glutamate | en_US |
dc.subject.other | Striatum | en_US |
dc.subject.other | Uptake | en_US |
dc.subject.other | Injury | en_US |
dc.title | Excitotoxic Brain Injury Suppresses Striatal High-Affinity Glutamate Uptake in Perinatal Rats | 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 | Departments of Pediatrics and Neurology, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | * The Neuroscience and Medical Scientist Training Program, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationother | † Departments of Neurology and Pediatrics, Johns Hopkins University and The Kennedy Research Institute, Baltimore, Maryland, U.S.A. | en_US |
dc.identifier.pmid | 1671587 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/65556/1/j.1471-4159.1991.tb02011.x.pdf | |
dc.identifier.doi | 10.1111/j.1471-4159.1991.tb02011.x | en_US |
dc.identifier.source | Journal of Neurochemistry | en_US |
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dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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