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The sensitivity of Helix aspersa neurones to injected calcium ions

The sensitivity of Helix aspersa neurones to injected calcium ions 1. 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 × 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Physiology Wiley

The sensitivity of Helix aspersa neurones to injected calcium ions

Meech, R. W.
The Journal of Physiology , Volume 237 (2) – Mar 1, 1974
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References (37)

Publisher
Wiley
Copyright
© 2014 The Physiological Society
ISSN
0022-3751
eISSN
1469-7793
DOI
10.1113/jphysiol.1974.sp010481
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Abstract

1. 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 × 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.

Journal

The Journal of Physiology – Wiley

Published: Mar 1, 1974

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