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.