Post-tetanic enhancement of stimulus-induced muscarinic afterdischarge in the rat superior cervical ganglion.
The enhancement of asynchronous muscarinic ganglionic firing which follows a preganglionic nerve stimulus volley by high frequency repetitive conditioning stimuli was studied in the rat isolated superior cervical ganglion. Muscarinic afterdischarge which occurred in chlorisondamine-blocked ganglia was enhanced for up to 1 hr after a 40 Hz conditioning volley lasting 7.5 to 30 sec. Enhancement did not occur when release of acetylcholine was blocked by reducing the calcium in the modified Krebs' solution or when magnesium or manganese chlorides were added to the saline during the conditioning period. Metabolic inhibitors, dinitrophenol, sodium azide and ouabain, blocked the enhancement process but not the asynchronous muscarinic firing. Phenytoin, 10(-6) M, did not reduce the enhancement of firing. Dopamine, 5 X 10(-5) M, had no effect on muscarinic afterdischarge, but dibutyryl cyclic adenosine 3':5'-monophosphate, 5 and 10 X 10(=3) M, caused a 43 and 53% increase in the maximum amplitude of afterdischarge. Dibutyryl cyclic guanosine 3':5'-monophosphate had no effect on post-tetanic enhancement or afterdischarge in concentrations up to 1 X 10(-3) M. A working hypothesis is proposed: following a conditioning stimulus, a prolonged postsynaptic change occurs which results in an increased responsiveness to muscarinic agonists, and this change probably involves a metabolic reaction since it is reduced by metabolic inhibitors. Evidence to support the concept that dopamine is a modulator of enhancement in the rat superior cervical ganglion was not obtained.
Post-tetanic enhancement of stimulus-induced muscarinic afterdischarge in the rat superior cervical ganglion. The enhancement of asynchronous muscarinic ganglionic firing which follows a preganglionic nerve stimulus volley by high frequency repetitive conditioning stimuli was studied in the rat isolated superior cervical ganglion. Muscarinic afterdischarge which occurred in chlorisondamine-blocked ganglia was enhanced for up to 1 hr after a 40 Hz conditioning volley lasting 7.5 to 30 sec. Enhancement did not occur when release of acetylcholine was blocked by reducing the calcium in the modified Krebs' solution or when magnesium or manganese chlorides were added to the saline during the conditioning period. Metabolic inhibitors, dinitrophenol, sodium azide and ouabain, blocked the enhancement process but not the asynchronous muscarinic firing. Phenytoin, 10(-6) M, did not reduce the enhancement of firing. Dopamine, 5 X 10(-5) M, had no effect on muscarinic afterdischarge, but dibutyryl cyclic adenosine 3':5'-monophosphate, 5 and 10 X 10(=3) M, caused a 43 and 53% increase in the maximum amplitude of afterdischarge. Dibutyryl cyclic guanosine 3':5'-monophosphate had no effect on post-tetanic enhancement or afterdischarge in concentrations up to 1 X 10(-3) M. A working hypothesis is proposed: following a conditioning stimulus, a prolonged postsynaptic change occurs which results in an increased responsiveness to muscarinic agonists, and this change probably involves a metabolic reaction since it is reduced by metabolic inhibitors. Evidence to support the concept that dopamine is a modulator of enhancement in the rat superior cervical ganglion was not obtained.