Interaction between nerve‐related acetylcholine and bath applied agonists at the frog end‐plate.

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Abstract
The interaction between acetylcholine (ACh) and carbachol (CCh) was studied at the frog [Rana esculenta] end-plate. The conditioning agonist, CCh, can cause desensitization (reduction of the ACh test response) and potentiation (increase of the test response). Nerve-evoked, end-plate currents (EPC), miniature EPC and slow responses to ACh iontophoresis can all be potentiated by bath or iontophoretically applied CCh. Since potentiation was particularly visible at low temperatures, most experiments were performed at 5-8.degree. C. Potentiation results in an increase of both EPC amplitude and EPC decay time. Potentiated EPC terminate with a slow tail, the amplitude of which shows a high voltage sensitivity. Potentiation increases with CCh concentration (range studied 0-100 .mu.M). It persists throughout the application of CCh, even when desensitization is apparently the dominant phenomenon. Cross-potentiation of ACh by CCh results from the formation of intermediate non-conducting CCh-receptor complexes which have a high probability of being subsequently activated by ACh, yielding a conducting ACh-CCh-receptor complex. Desensitization induced by fast bath application of CCh (or ACh) develops in 2 phases and can be fitted by the sum of 2 exponentials. Their time constants are in the second and the minute range, respectively. The possibility that the slow phase is linked to the presence of agonist inside the cell is rejected.