Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1983-6-23
pubmed:abstractText
The role of spinal pathways in the regulation of tyrosine hydroxylase activity (ATHA) in the adrenal medulla was characterized in adult rats with surgical transection of the upper thoracic cord. The animals received injections of centrally active agonists, which could then act on the sympathoadrenal preganglionic neurons isolated from their supraspinal afferents. All agonists tested produced distinct increases of tyrosine hydroxylase activity in rats with a surgical sham operation. The injection of quipazine or oxotremorine into spinalized rats led to decreased tyrosine hydroxylase activity. Clonidine and several dopamine agonists did not affect tyrosine hydroxylase activity. Considering the mechanism of the observed changes in tyrosine hydroxylase activity it is concluded that the changes are mediated by neural pathways and that variations in the secretion of adrenocorticotrophic hormone (ACTH) do not play a role. The results suggest (a) that there are serotonergic and cholinergic (muscarinic) receptors in the lower thoracic cord generating a net inhibitory action on tyrosine hydroxylase activity; and (b) that increases of tyrosine hydroxylase activity mediated by dopaminergic drugs probably originate from areas rostral to the thoracic cord. It is possible that an alpha-adrenergic system participates in the regulation of tyrosine hydroxylase activity in the adrenal medulla.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0028-3908
pubmed:author
pubmed:issnType
Print
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
45-53
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1983
pubmed:articleTitle
Participation of spinal monoaminergic and cholinergic systems in the regulation of adrenal tyrosine hydroxylase.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't