ABSTRACT
The findings was confirmed that there is a "rebound" increase of stored acetylcholine (ACh) in cat superior cervical ganglia conditioned by prolonged preganglionic stimulation at a frequency high enough to cause initial depletion of the store. Ganglia removed immediately after 60 min of continuous or interrupted stimulation at 50 Hz, with chloralose as anesthetic, contained about 30% more ACh than their unconditioned controls; the rebound rose to about 60% after 15 min of rest and then subsided with an apparent half-time of about 2 h. Tests with hemicholinium, combined with hexamethonium or tubocurarine, showed that rebound ACh was located presynaptically and could be released by nerve impulses; but conditioned ganglia perfused with an eserine-containing medium did not release more ACh than their unconditioned controls, except in circumstances in which the mobilization of ACh from a reserve store appeared to be the rate-limiting process for release. The appearance of rebound ACh during and after conditioning stimulation was suppressed by hexamethonium and by tubocurarine, neither of which has much effect on ACh turnover in ganglia excited at lower frequencies, but not only by atropine, noradrenaline, or phenoxybenzamine. The formation of rebound ACH is thus contingent on the postsynaptic nicotinic response to released ACh, and may represent an augmentation of the transmitter store in structures remote from the release sites.
