Linked Life Data

7499548

Source:http://linkedlifedata.com/resource/pubmed/id/7499548

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1996-1-18
pubmed:abstractText
Experimental lesions have been widely used to induce neuronal degeneration and to test the ability to trophic molecules to prevent lesion-induced alterations, but these studies have not demonstrated unequivocally that afflicted neurons die as a result of these manipulations. The documentation of neuronal death in the above-described models and the time when it occurs after injury are crucial for the interpretation of trophic effects. In the present study, we combined multiple approaches to investigate the nature of retrograde neuronal changes in cholinergic neurons of the medial septal nucleus (MSN) after complete, unilateral transection of the fimbria-fornix (F-F). Projections neurons of the MSN were prelabeled with the fluorescent tracer Fluoro-gold (FG) 1 week prior to lesion. By counting both FG-labeled and choline acetyltransferase (ChAT)-immunoreactive neurons in the MSN at multiple time points postaxotomy, we differentiated the phenotypic response to injury from the degenerative process and established a critical time between the third and fourth weeks postaxotomy, during which approximately 50% of fluorescent perikarya disappear. Working in the previous time window, we identified dying cells by electron microscopy (EM) and terminal transferase-mediated (TdT) deoxyuridine triphosphate (d-UTP)-biotin nick end labeling (TUNEL) and showed that MSN neurons die via apoptosis, beginning at 16 days postaxotomy. An additional group of animals was allowed to survive for 1 month (i.e., 10 days after cell death has been completed); during this period, animals were treated with intraventricular nerve growth factor (NGF). Quantitative analysis of surviving cholinergic perikarya showed that NGF prevented degeneration of the majority of neurons. In concert, the results of the present study establish that NGF does not merely protect the phenotype but also prevents cell death in lesioned central cholinergic neurons.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0021-9967
pubmed:author
pubmed:issnType
Print
pubmed:day
4
pubmed:volume
359
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
573-85
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Nerve growth factor prevents apoptotic cell death in injured central cholinergic neurons.
pubmed:affiliation
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, Maryland 21205, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.