The inference that lithium acts by altering intracellular calcium functions is supported by the three areas considered above. First, recent work in other laboratories has broadened the range of lithium actions on calcium-dependent physiological functions. Second, a theoretical analysis of the coupling of calcium transport to the triphosphoinositide response presents a plausible mechanism by which lithium could limit the damage caused by deficient calcium transport. Third, we have recently reported that there is a direct enhancement of the calmodulin-activated membrane-bound calcium pump in lithium-treated bipolar subjects.
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Herbert L. Meltzer (1990) studied this question.
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