Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1989-1-31
pubmed:abstractText
Peripheral sympathetic neurons are thought to provide trophic regulatory signals for development of adrenergic target tissues. In the current study, we destroyed central catecholaminergic pathways in the neonatal rat by intracisternal administration of 6-hydroxydopamine, which compromises sympathetic tone without ablating peripheral nerve terminals. Measurements of norepinephrine levels and turnover confirmed the effectiveness of the treatment in projections to heart, lung and kidney. The impairment of sympathetic tone was associated with a deficit in cardiac beta adrenergic receptor binding capabilities; in contrast, binding sites in the lung were unaffected and renal receptors were up-regulated. Similarly, intracisternal administration of 6-hydroxydopamine produced tissue-selective alterations in ornithine decarboxylase activity and levels of the polyamines. These results support the view that neural activity exerts an influence on the biochemical development of sympathetic target tissues; however, other trophic factors may derive from the presence of intact nerve terminals themselves, as distinct from activity.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
247
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
975-82
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Neonatal central catecholaminergic lesions with intracisternal 6-hydroxydopamine: effects on development of presynaptic and postsynaptic components of peripheral sympathetic pathways and on the ornithine decarboxylase/polyamine system in heart, lung and kidney.
pubmed:affiliation
Department of Pharmacology, Duke University Medical Center, Durham, North Carolina.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.