These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Effect of monoamine uptake inhibitors on norepinephrine-stimulated phosphatidylinositol hydrolysis in rat cortex. Author: Mosaddeghi M, Moerschbaecher JM, Gonzales RA. Journal: Biochem Pharmacol; 1989 Jan 15; 38(2):257-62. PubMed ID: 2536541. Abstract: The effects of the monoamine uptake inhibitors cocaine, nisoxetine, and desipramine (DMI) on norepinephrine (NE) stimulated phosphatidylinositol (PI) hydrolysis were investigated. Rat cortical tissue slices were labeled with [3H]inositol. Slices were then stimulated, in vitro, with NE in LiCl containing buffer in the presence and absence of monoamine uptake inhibitors. Cocaine and nisoxetine, but not DMI, potentiated NE-stimulated PI hydrolysis with a significant decrease in the EC50. Nisoxetine appeared to be more potent than cocaine with respect to the potentiation of NE-stimulated PI hydrolysis. The potentiating effect of cocaine was biphasic and dependent upon the concentrations of cocaine and NE. The NE concentration-effect curve was shifted to the right 100-fold in the presence of 0.1 microM prazosin. Cocaine at 10 microM did not potentiate NE-stimulated PI hydrolysis in the presence of 0.1 microM prazosin. Cocaine at 10 microM did not affect significantly the binding of [3H]prazosin or the NE-[3H]prazosin competition binding to cortical membranes. The results suggest that NE-uptake inhibition by cocaine and nisoxetine is the mechanism for the enhancement of NE-stimulated PI hydrolysis.[Abstract] [Full Text] [Related] [New Search]