Key points are not available for this paper at this time.
When calcium chloride was injected into Helix aspersa neurones there was a fall in membrane resistance and the membrane potential became hyperpolarized.2. The reversal potential of the response was dependent on the concentration of potassium in the external solution.3. Injection of a calcium-EGTA buffer containing 9 x 10(-7)M free calcium reduced the membrane resistance by 25%. When calcium chloride was injected it was necessary to increase the total intracellular calcium concentration by about 10(-3)M to produce similar change of resistance.4. In sodium-free (Tris) solution there was a slow fall of membrane resistance as if the intracellular calcium concentration had increased. There was a similar resistance change in the presence of 2,4-dinitrophenol and iodoacetate.5. A series of repetitive depolarizing pulses produced a long lasting reduction in membrane resistance which was enhanced by 2,4-dinitrophenol and iodoacetate.6. It is concluded that (a) injection of calcium causes an increase in potassium permeability, (b) the injected calcium is rapidly pumped from the cytoplasm by a sodium-dependent mechanism and by mitochondria, and (c) 1-2 msec depolarizing pulses stimulate an influx of calcium. This influx is rapid enough to trigger potassium activation during an action potential.
Robert W. Meech (Fri,) studied this question.