IMMOBILIZATION STRESS ELEVATES GENE-EXPRESSION FOR CATECHOLAMINE BIOSYNTHETIC-ENZYMES AND SOME NEUROPEPTIDES IN RAT SYMPATHETIC-GANGLIA - EFFECTS OF ADRENOCORTICOTROPIN AND GLUCOCORTICOIDS

Citation
B. Nankova et al., IMMOBILIZATION STRESS ELEVATES GENE-EXPRESSION FOR CATECHOLAMINE BIOSYNTHETIC-ENZYMES AND SOME NEUROPEPTIDES IN RAT SYMPATHETIC-GANGLIA - EFFECTS OF ADRENOCORTICOTROPIN AND GLUCOCORTICOIDS, Endocrinology, 137(12), 1996, pp. 5597-5604
Citations number
50
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
00137227
Volume
137
Issue
12
Year of publication
1996
Pages
5597 - 5604
Database
ISI
SICI code
0013-7227(1996)137:12<5597:ISEGFC>2.0.ZU;2-I
Abstract
Sympathetic ganglia are the major contributors to the stress-elicited rise in circulating norepinephrine, enkephalins, and neuropeptide Y. H ere we examined the effect of immobilization stress and treatment with ACTH and glucocorticoids on messenger RNA (mRNA) levels for tyrosine hydroxylase (TH), dopamine beta-hydroxylase (DBH), preproneuropeptide Y (pre-NPY), and proenkephalin in rat superior cervical ganglia(SCG) a nd in stellate ganglia. Our results show a severalfold increase in the relative abundance of TH and NPY mRNAs in response to a single immobi lization. Repeated stress elevated expression of all the genes studied and increased TH immunoreactivity in both ganglia. The effect of stre ss was more pronounced in SCG. Prolonged cortisol administration faile d to alter the mRNA levels of TH, DBH, and NPY in control animals but attenuated the response to stress. In contrast, TH and DBH mRNA levels in the SCG, but not in adrenal medulla, were elevated by ACTH adminis tration, similar to the levels attained after immobilization. The resu lts revealed that the regulation of gene expression in response to imm obilization stress in sympathetic neurons differs from the regulation in adrenal medulla. The study implicates hormonal involvement in the s tress-induced changes in TH, DBH, NPY, and proenkephalin gene expressi on in sympathetic ganglia.