Abstract
Basal and drug-induced levels of cAMP were determined in cortical slices from mice which were homozygous for the tottering ( tg/tg) gene defect as well as from co-isogenic controls (+/+). Basal levels of cAMP were 77±16% higher in tg/tg slices compared to the controls. This difference was abolished by exposure of the slices to propranolol, a β-adrenergic receptor antagonist. Both isoproterenol and veratridine stimulated cAMP formation, but only small differences were observed in the cAMP levels in g/tg and +/+ slices after this treatment. Of the veratridine-dependent increase in cAMP, approximately 40% was blocked by propranolol treatment of slices from both strains. The results suggest that a higher level of endogenous norepinephrine release in tottering mice contributes to an elevation of basal cAMP levels.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
