Isolated Helix neurons were internally perfused under voltage-clamp, with drugs applied by the 'concentration clamp' which allowed an extremely rapid switching of the external solution. 4-Aminopyridine (4-AP) at more than 3 X 10(-4) M induced a chloride current (ICl) which could be blocked by D-tubocurarine. Acetylcholine (ACh) also induced ICl which was similarly blocked. Simultaneous application of 4-AP and ACh resulted in potentiation of ICl over the sum of respective currents. When preceded by either one, the other ICl was reduced in size, showing cross-desensitization. These data indicate that 4-AP activates ICl by binding to the cholinergic receptors, and reduces ACh-induced ICl by desensitizing a common receptor-channel complex.
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