rdf:type |
|
lifeskim:mentions |
umls-concept:C0020944,
umls-concept:C0035696,
umls-concept:C0038435,
umls-concept:C0041491,
umls-concept:C0150312,
umls-concept:C0152060,
umls-concept:C0205171,
umls-concept:C0205263,
umls-concept:C0242897,
umls-concept:C0521428,
umls-concept:C1709305
|
pubmed:issue |
1
|
pubmed:dateCreated |
1996-1-24
|
pubmed:abstractText |
Immobilization (IMO) stress elevates plasma catecholamines and increases tyrosine hydroxylase (TH) gene expression in rat adrenals. This study examined the mechanism(s) of IMO-induced changes in adrenal TH mRNA levels. Innervation of the adrenal medulla is predominantly cholinergic and splanchnicotomy as well as nicotinic receptor antagonists prevent the cold-induced rise in TH mRNA levels. In this study, the IMO-induced rise in plasma catecholamines, but not TH mRNA levels, was reduced by the antagonist chlorisondamine. Muscarinic antagonist atropine also did not prevent the IMO stress-elicited rise in TH mRNA. Furthermore, denervation of the adrenals by unilateral splanchnicotomy did not block the IMO-induced rise in TH mRNA but completely prevented the induction of neuropeptide Y mRNA. These results suggest that (1) the large increase in adrenal TH gene expression elicited by a single IMO stress is not regulated via cholinergic receptors or splanchnic innervation, and (2) there is a dissociation between regulatory mechanisms of catecholamine secretion and elevation of TH gene expression in the adrenal medulla of rats during IMO stress.
|
pubmed:grant |
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jan
|
pubmed:issn |
0022-3042
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
66
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
138-46
|
pubmed:dateRevised |
2008-11-21
|
pubmed:meshHeading |
pubmed-meshheading:8522945-Adrenal Medulla,
pubmed-meshheading:8522945-Animals,
pubmed-meshheading:8522945-Atropine,
pubmed-meshheading:8522945-Catecholamines,
pubmed-meshheading:8522945-Chlorisondamine,
pubmed-meshheading:8522945-Cholinergic Antagonists,
pubmed-meshheading:8522945-Cold Temperature,
pubmed-meshheading:8522945-Enzyme Induction,
pubmed-meshheading:8522945-Immobilization,
pubmed-meshheading:8522945-Male,
pubmed-meshheading:8522945-Muscarinic Antagonists,
pubmed-meshheading:8522945-Neuropeptide Y,
pubmed-meshheading:8522945-Nicotinic Antagonists,
pubmed-meshheading:8522945-RNA, Messenger,
pubmed-meshheading:8522945-Rats,
pubmed-meshheading:8522945-Rats, Sprague-Dawley,
pubmed-meshheading:8522945-Specific Pathogen-Free Organisms,
pubmed-meshheading:8522945-Splanchnic Nerves,
pubmed-meshheading:8522945-Stress, Physiological,
pubmed-meshheading:8522945-Sympathectomy,
pubmed-meshheading:8522945-Tyrosine 3-Monooxygenase
|
pubmed:year |
1996
|
pubmed:articleTitle |
Induction of adrenal tyrosine hydroxylase mRNA by single immobilization stress occurs even after splanchnic transection and in the presence of cholinergic antagonists.
|
pubmed:affiliation |
Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland, USA.
|
pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
|