Intracellular calcium and extra-retinal photoreception of Aplysia Giant neurons.

The early or "instantaneous" current-voltage relationship for the light-activated potassium current in Aplysia giant neurons was linear during the first second of illumination. However, the light current was greatly reduced or abolished by prolonged hyperpolarization. It was also greatly reduced by the injection of calcium EGTA buffers having calcium activities of 5.6 X 10(-8) M and simulated by injecting buffers with calcium activities of 2.8-5.6 X 10(-7) M. Removal of calcium from the extracellular fluid had no effect. Both the light- and calcium-activated outward potassium currents were reduced by tetraethylammonium (TEA) ions. The light current was not affected by substituting rubidium for potassium nor by substituting either lithium or Tris for sodium. The calcium-activated potassium current persisted when the neuron was cooled to 5 degrees C. However, the light response could no longer be elicited. Light hyperpolarizes Aplysia neurons probably by increasing intracellular calcium activity two-to six-fold which activates a membrane potassium conductance. Calcium levels appear to be restored within the cell and are energy dependent. The light-activated release of calcium is inhibited by cooling. The body wall of Aplysia transmits enough visible or 500 nm light to hyperpolarize some Aplysia giant neurons under ambient conditons. These neurons may be involved in the extraretinal light entrainment that occurs in Aplysia.