Linked Life Data

10188935

Source:http://linkedlifedata.com/resource/pubmed/id/10188935

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-9-8
pubmed:abstractText
Unilateral neurotoxin lesion of rat caudate-putamen and globus pallidus resulted in delayed, transneuronal degeneration of GABAergic substantia nigra pars reticulata neurons. To explore whether the disinhibition of endogenous glutamate excitatory input played a role in the degeneration of substantia nigra pars reticulata neurons, animals with unilateral striatal-pallidal lesions received three daily intraperitoneal injections of either dizocilpine maleate (MK-801, 1 or 10 mg/kg), an N-methyl-D-aspartate glutamate receptor blocker, or 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)quinoxaline (NBQX, 30 mg/kg), an alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptor blocker, that began 24 h after the striatal-pallidal neurotoxin lesion. Drug treatment affected neither the volume of the initial lesion nor the volume of striatal-pallidal glial fibrillary acidic protein immunoreactivity. Neuron number in the substantia nigra pars reticulata ipsilateral to the lesioned striatopallidum was reduced on average by 37% in untreated control rats, in low dose MK-801, and NBQX-treated rats (P<0.0001). However, in animals treated with high doses of MK-801 there was no difference in the number of neurons in the substantia nigra pars reticulata ipsilateral or contralateral to the neurotoxin lesion. These data demonstrate that dose-related treatment with N-methyl-D-aspartate glutamate receptor blockers protects substantia nigra pars reticulata neurons, and suggests that glutamatergic mechanisms play a role in delayed transneuronal degeneration.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
90
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
79-85
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10188935-Animals, pubmed-meshheading:10188935-Corpus Striatum, pubmed-meshheading:10188935-Dizocilpine Maleate, pubmed-meshheading:10188935-Dose-Response Relationship, Drug, pubmed-meshheading:10188935-Drug Evaluation, Preclinical, pubmed-meshheading:10188935-Excitatory Amino Acid Antagonists, pubmed-meshheading:10188935-Globus Pallidus, pubmed-meshheading:10188935-Ibotenic Acid, pubmed-meshheading:10188935-Male, pubmed-meshheading:10188935-Nerve Degeneration, pubmed-meshheading:10188935-Neurons, pubmed-meshheading:10188935-Neuroprotective Agents, pubmed-meshheading:10188935-Neurotoxins, pubmed-meshheading:10188935-Putamen, pubmed-meshheading:10188935-Quinoxalines, pubmed-meshheading:10188935-Rats, pubmed-meshheading:10188935-Rats, Wistar, pubmed-meshheading:10188935-Receptors, AMPA, pubmed-meshheading:10188935-Receptors, Glutamate, pubmed-meshheading:10188935-Substantia Nigra
pubmed:year
1999
pubmed:articleTitle
Dizocilpine maleate, MK-801, but not 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)quinoxaline, NBQX, prevents transneuronal degeneration of nigral neurons after neurotoxic striatal-pallidal lesion.
pubmed:affiliation
Department of Neurology and Neuroscience, Cornell University Medical College at the Burke Medical Research Institute, White Plains, NY 10605, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't