Evidence for a role of noradrenergic neurons in the increase in concentration of preprocholecystokinin-mRNA after cerebral cortex injury in rats.
A knife cut injuring the meninges and the upper layers of rat neocortex transiently increases the levels of preprocholecystokinin-mRNA in the whole ipsilateral cortex. 48 h after the injury, the rise in gene expression was reduced by the edema-induced increase in tissue pressure which develops after the trauma. The beta-adrenoceptor antagonists alprenolol (4 mg/kg) and propranolol (1 mg/kg), given i.m. 30 min prior to the injury, reduced the increase by 75.6 and 100%, respectively. In contrast, blockade of alpha-adrenoceptors as well as of dopamine and serotonin receptors by respective antagonists did not affect the injury-induced increase in levels of preprocholecystokinin-mRNA. These results suggest that noradrenergic neurons can contribute via stimulation of beta-adrenoceptors to the initiation of the injury-induced increase in preprocholecystokinin gene expression.
Olenik
C
C
Department of Pharmacology, University of Freiburg, Germany.
Götz
E
E
Uhl
A
A
Mondeh
J D
JD
Meyer
D K
DK
D000818:Animals; D002540:Cerebral Cortex / Q000293:injuries*; D002766:Cholecystokinin / Q000235:genetics*; D008297:Male; D009474:Neurons / Q000502:physiology*; D009638:Norepinephrine / Q000502:physiology*; D011498:Protein Precursors / Q000235:genetics*; D012333:RNA, Messenger / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar
D011498:Protein Precursors; D012333:RNA, Messenger; C042082:preprocholecystokinin; D002766:Cholecystokinin; D009638:Norepinephrine