Differential time- and dose-related effects of haemorrhage on tyrosine hydroxylase and neuropeptide Y mRNA expression in medullary catecholamine neurons

Citation
Rkw. Chan et Pe. Sawchenko, Differential time- and dose-related effects of haemorrhage on tyrosine hydroxylase and neuropeptide Y mRNA expression in medullary catecholamine neurons, EUR J NEURO, 10(12), 1998, pp. 3747-3758
Citations number
73
Categorie Soggetti
Neurosciences & Behavoir
Journal title
EUROPEAN JOURNAL OF NEUROSCIENCE
ISSN journal
0953816X → ACNP
Volume
10
Issue
12
Year of publication
1998
Pages
3747 - 3758
Database
ISI
SICI code
0953-816X(199812)10:12<3747:DTADEO>2.0.ZU;2-5
Abstract
Hypotensive haemorrhage induces nuclear Fos expression and upregulates tyro sine hydroxylase (TH) mRNA in catecholamine-containing cell groups of the r at medulla oblongata. To shed light on the significance of the coexistence of neuropeptide Y (NPY) in aminergic neurons, the impact of graded levels o f haemorrhage on temporal changes in the expression of TH and NPY mRNAs was compared; concurrent staining for Fos permitted comparisons between cells that ostensibly were and were not targeted by the stimulus. A 15% haemorrha ge provoked increased NPY expression in all medullary catecholamine cell gr oups except the A2; these changes were detected predominantly in Fos-immuno reactive neurons (Fos-ir) at later (2-4 h) time points, Upregulation of TH and NPY mRNAs in Fos-ir neurons followed distinct time courses, with NPY re sponses peaking more rapidly, particularly in the C1 and C2 cell groups. Ad renergic cell groups displayed greater maximal increases in NPY expression than the Al noradrenergic cell group while the converse was true of TH mRNA response. Increasing the severity of haemorrhage resulted in more pronounc ed increases in both mRNA responses in each aminergic region, These finding s indicate that haemorrhage differentially affects TH and NPY expression in medullary catecholamine cell groups that participate in the maintenance of cardiovascular homeostasis. The differential nature of these responses sug gests them not to be a simple consequence of metabolic alterations pursuant to increased synaptic activity. The prompt and robust NPY mRNA responses i n adrenergic neurons suggests a mechanism by which peptide content of these cell groups' terminal projections is defended.