Effect of acetylcholine on ventrocaudal sensory neurons in the pleural ganglia of Aplysia.

1. The effects of acetylcholine (ACh) on the soma of cultured ventrocaudal sensory neurons from the pleural ganglia of Aplysia kurodai were characterized. 2. Whole-cell recording was used for current and voltage clamping. ACh and other drugs were microapplied to the membranes of the cultured neurons. 3. Microapplication of ACh induced an outward current mediated by a conductance increase. No desensitization to repeated applications of ACh was detected. The threshold was 10(-7) M and the maximum response was at 10(-5) M. 4. The reversal potential in normal seawater is -80 mV, close to the K+ equilibrium potential. Increasing [K+]0 shifted the reversal potential by the amount predicted by the Nernst equation. Altering [Cl-]0 did not affect the reversal potential. Thus ACh opens a potassium channel in these sensory neurons and may act as a neurotransmitter on those neurons. 5. Atropine and d-tubocurarine partially blocked the ACh response. Hexamethonium had no obvious effect on this response. Tetraethylammonium reduced the response to 22% of control. Carbamylcholine and arecoline induced outward currents that were 71 and 12%, respectively, of the response to ACh. Nicotine and muscarine had almost no effect. 6. The ACh response was reduced by prior application of serotonin (5HT). The ACh response was also reduced by bath-applied 5HT, forskolin, and isobutylmethylxanthine. These data suggest that ACh activates an "S-like" channel in the ventrocaudal sensory neurons.