Ganglionic blockade by d-amphetamine.
The actions of d-amphetamine on ganglionic transmission in the isolated stellate ganglion of the hamster were observed. Blockade of the compound action potential by d-amphetamine had a slow onset with an onset half-time of 2-5 min. The concentration-blockade relationship for d-amphetamine was not shifted by phentolamine (10(-5) M) or propranolol (10(-6) M). The blockade was frequency-dependent, and the frequency-dependence was suppressed by atropine (10(-6) M). It was suggested that the frequency-dependence of d-amphetamine involved a muscarinic mechanism. In support of this suggestion, the afterdischarges from repetitive stimulation in hexamethonium were relatively insensitive to d-amphetamine. Also afterdischarges could be recorded after repetitive stimulation in 10(-4) M d-amphetamine, without hexamethonium. High concentrations of d-amphetamine (10(-3) M) induced discharges in the postganglionic nerve and potentiated the discharges from the cholinergic agonists, DMPP and McN-A-343. Tolerance rapidly developed to these stimulatory effects. These results indicate that ganglionic blockade by d-amphetamine is produced by a different mechanism than ganglionic blockade by the catecholamines.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D006224:Cricetinae; D003913:Dextroamphetamine / Q000494:pharmacology*; D004347:Drug Interactions; D004558:Electric Stimulation; D008647:Mesocricetus; D009433:Neural Inhibition / Q000187:drug effects; D010277:Parasympathomimetics / Q000494:pharmacology; D013233:Stellate Ganglion / Q000187:drug effects*; D009435:Synaptic Transmission / Q000187:drug effects
D010277:Parasympathomimetics; D003913:Dextroamphetamine