Electron microscopic studies on the effect of long-term hypercalcemia on the thyroid parafollicular cell and the parathyroid cell of rats.

A cell type different from the follicular cells of the thyroid was discovered by BABER (1876) and named "parafollicular cell" by NONIDEZ (1932). As to the function of this cells, different opinions were proposed. It was regarded, for instance, as a degenerated follicular epithelial cell, an undifferentiated follicular epithelial cell, a neuroepithelial cell without any relationship to the follicular epithelial cell and a mesenchymal cell. COPP et al. (1962) discovered a calcium lowering factor in the parathyroid by perfusion experiment with calcium and named it "calcitonin." HIRSCH et al. (1963) reported that this factor does not originate from the parathyroid but from the thyroid gland and named it "thyrocalcitonin." BUSSOLATI and PEARSE (1967) demonstrated that the origin of the thyrocalcitonin is a parafollicular cell by the immunohistological method. Since then, numerous papers (HARGIS et al., 1966; NUNEZ, 1967; FOSTER 1967; PEARSE and CARVALHEIRA, 1967; CAPEN and YOUNG, 1967; MEYER and ABDEL-BARI, 1968; EKHOLM and ERICSON, 1968; ERICSON, 1968; ROHR and HASLER, 1968; KAMEDA, 1968; YOUNG et al., 1968; KRACHT, 1964; BRAUNSTEIN and STEPHENS, 1968; TASHJIAN, 1969; NANBA and FUJITA, 1969; LEE et al., 1969) have dealt with the parafollicular cell, using immunochemical and morphological methods. Concerning the relationship between intracellular specific granules and thyrocalcitonin, morphological studies have been made by several authors (MATSUZAWA, 1966, BAUER and TEITELBAUM, 1966). YOUNG et al. (1968) reported that hypercalcemia increases the number of granules, whereas several other authors (MATSUZAWA, 1966; KAMEDA, 1968; ERICSON, 1968; NANBA and FUJITA, 1969) found that they are markedly reduced in the corresponding conditions. These papers deal with cases of short time hypercalcemia caused by a single injection of calcium. However, the present author, who considered that it is difficult to obtain clear results by a single injection of calcium, observed fine structural changes of the parafollicular cell in the long-term hypercalcemic rat. Several years ago, homeostasis of the calcium content in the blood serum was considered to be regulated by only the parathormone secreted by the parathyroid. However, the thyroid gland as well as the parathyroid gland must be observed to morphologically study the calcium metabolism, as CAPEN and YOUNG (1967) did. In the present paper, the author describes cytological changes of both the parafollicular cell and the parathyroid cell of long-term hypercalcemic rats.