These results may be interpreted as follows: Calcium entry into R15 is brought about by hypoxia. The amount of intracellular calcium is probably buffered by the endoplasmic reticulum and the mitochondria whose processes of oxidative phosphorylation exchange protons for Ca2 + ions. (12, 13, 14) It is known that calcium entry into molluscan neurons inactivates the Ca2 + current and that potassium conductance is increased by higher levels of intracellular Ca2 +. (8, 9, 10, 26) Therefore, inactivation of the calcium channel through entry explains why the spike amplitude is depressed without affecting the threshold for activation as shown in Table 1. Secondly, an increased potassium conductance resulting from an increase in intracellular Ca2 + accounts for the membrane hyperpolarization. Little effect, then, is seen on the level of intracellular potassium ion activity (aiK +) since the membrane potential becomes more permeable to potassium and hyperpolarizes. Therefore, the value of EK is relatively unchanged during hypoxia; yet the values of the membrane potential (Em) hyperpolarize corresponding to an increase in potassium conductance. In summary, not only is the cyclical bursting pattern of R15 altered by reduced oxygen tensions in the suffusate but also each spike is depressed in amplitude because of an overabundant calcium entry during hypoxia. Presumably, the additional minute amounts of calcium are buffered by uptake into the mitochondria and endoplasmic reticulum, but there may be a significant increase in intracellular calcium enough so that the pump is not sufficient to move calcium externally without the energy resulting from the driving force of the sodium equilibrium potential (ENa).(ABSTRACT TRUNCATED AT 250 WORDS)