Year-end Sale % OFF 
Abstract
Phosphatidylinositol (PI) breakdown in rat cerebral cortex is stimulated by serotonin (5-HT), acting via 5-HT 2 and possibly 5-HT 3 receptors and by acetylcholine or carbachol, acting via muscarinic M1 and M3 receptors. Serotoninergic neurons have been described as tonically inhibiting cortical acetylcholine release. We studied the effects of subchronic pretreatment with high doses of d-fenfluramine (10 mg/kg, i.p., daily for 4 days), which releases 5-HT and blocks its reuptake, on 5-HT- and carbachol-stimulated PI breakdown, as measured by [ 3H]inositolmonophosphate ([ 3H]IP1) accumulation in cortical miniprisms. This pretreatment decreased 5-HT-stimulated [ 3H]IP1 accumulation, suggesting that a prolonged increase of 5-HT in the synaptic cleft reduces the activity of the transducing systems used by postsynaptic 5-HT receptors. Carbachol-stimulated PI breakdown was unaltered by pretreatment with d-fenfluramine. Pretreatment with a single dose of p-chloroamphetamine (5 mg/kg), a serotoninergic neurotoxin, which depleted cortical 5-HT by 85%, did not change [ 3H]IP1 accumulation after stimulation by 5-HT or by the muscarinic agonist carbachol. Subchronic pretreatment, which depleted cortical 5-HT by 90%, decreased both 5-HT- and carbachol-stimulated [ 3H]IP1 accumulation. The mechanism by which p-chloroamphetamine, but not d-fenfluramine, diminishes the PI response to carbachol might involve impairment of the tonic serotoninergic inhibition of acetylcholine release.
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.
