Linked Life Data

1379936

Source:http://linkedlifedata.com/resource/pubmed/id/1379936

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1992-9-11
pubmed:abstractText
The question of how the cerebral cortex responds over time to changes in cortical neuronal number was addressed by inducing excitotoxic cortical neuronal loss, either alone or followed by homotypic fetal cortical cell suspension grafts, in adult rats. Following neuronal cell loss, rapid gliosis and inflammation temporarily maintained tissue volume. As gliosis subsided, tissue shrinkage occurred until the ratio of glia to neurons approached that of normal neocortex. After neuronal loss, total cortical glutamate uptake and glutamic acid decarboxylase activity dropped markedly and remained low, and there was a gradual but considerable reduction in the total size of afferent fiber networks. However, when expressed as concentrations per unit of tissue or protein, histological and neurochemical cortical markers showed increases during the phase of tissue shrinkage and in the long-term equilibrated to near normal levels. Retrograde tracing studies showed that the reduction in total afferent fiber network is accompanied by the atrophy of afferent neuronal cell bodies. Grafts of fetal cortical cells placed after excitotoxic lesions provided long-term reconstitution of cortical tissue mass, maintained afferent fiber systems, and prevented both the atrophy and surrounding cellular gliosis of some afferent neuronal cell bodies for over a year, but were unable to innervate the main cortical target regions in the host. Thus after neuronal loss or replacement, the adult cerebral neocortex and its afferent systems remodel to a density of neurons, glia, and afferent fibers similar to that found in intact tissue, illustrating structural plasticity toward a dynamic equilibrium.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0014-4886
pubmed:author
pubmed:issnType
Print
pubmed:volume
117
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
151-75
pubmed:dateRevised
2009-9-29
pubmed:meshHeading
pubmed-meshheading:1379936-Afferent Pathways, pubmed-meshheading:1379936-Analysis of Variance, pubmed-meshheading:1379936-Animals, pubmed-meshheading:1379936-Axonal Transport, pubmed-meshheading:1379936-Cerebral Cortex, pubmed-meshheading:1379936-Choline O-Acetyltransferase, pubmed-meshheading:1379936-Female, pubmed-meshheading:1379936-Glutamate Decarboxylase, pubmed-meshheading:1379936-Glutamates, pubmed-meshheading:1379936-Glutamic Acid, pubmed-meshheading:1379936-Kainic Acid, pubmed-meshheading:1379936-N-Methylaspartate, pubmed-meshheading:1379936-Nerve Degeneration, pubmed-meshheading:1379936-Nerve Regeneration, pubmed-meshheading:1379936-Neurons, pubmed-meshheading:1379936-Neurotoxins, pubmed-meshheading:1379936-Norepinephrine, pubmed-meshheading:1379936-Rats, pubmed-meshheading:1379936-Rats, Inbred Strains, pubmed-meshheading:1379936-Serotonin, pubmed-meshheading:1379936-Sympathectomy
pubmed:year
1992
pubmed:articleTitle
Neuronal loss or replacement in the injured adult cerebral neocortex induces extensive remodeling of intrinsic and afferent neural systems.
pubmed:affiliation
Department of Neurology, Harvard Medical School, McLean Hospital, Belmont, MA 02178.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't