An increase in brain and peripheral nerve calcium has been demonstrated in dogs with acute uremia and was found to be induced by excess parathyroid hormone in blood. This abnormality is associated with deranged electroencephalogram (EEG) and motor nerve conduction velocity. Prior removal of parathyroid glands prevents the accumulation of calcium in brain and normalized EEG. Studies will be carried out in dogs and rats to evaluate the mechanisms by which calcium enters the brain and crosses the blood brain barrier in states with excess parathyroid hormone. In addition, the localization of calcium with the brain cell on the nerve fiber will be examined. More specifically, the following will be done: 1. Investigate whether high calcium content in brain or nerve is present in states with chronic and prolonged hyperparathyroidism. 2. Determine the relation between blood levels of PTH and brain and nerve calcium. 3. Examine the sites whether the accumulated calcium in brain or nerve is located. 4. Delineate the component of the blood brain barrier that is affected by PTH and allows the entry of calcium into brain. 5. Investigate whether PTH crosses the blood-CSF interface and whether PTH enters the brain. 6. Evaluate whether PTH stimulates a brain adenylate cyclase-cyclic AMP system or it enhances synthesis of a calcium binding protein. 7. Examine whether calcitonin can antagonize the effect of PTH on brain or nerve calcium.