The literature on interrelationships among thyroid, C cells and catecholaminergic systems in the brain is reviewed. The main available data can be summarized as follows. Monoamines and their precursors (l-DOPA, DA, NA, A, 5-HT) are stimulatory to iodine incorporation and iodothyronine synthesis in the calf thyroid. DA and NA concentrations in anterior hypothalamus influence TSH secretion from hypophysis and TRH secretion from hypothalamus. Thyroxine increases NA and DA turnover in mouse brain and subsequently it increases CA receptor sensitivity. Such effects are more evident for DA than NA. Chorea occurs in a small percentage of patients with hyperthyroidism. Klawans suggested that in man hyperthyroidism increases the sensitivity of striatal receptor sites to DA. Analogously, apomorphine induces stereotyped behavior in hyperthyroid guinea pigs. CSF HVA is reduced also in patients with hyperthyroid and without chorea. L-triiodothyronine and TSH enhance the therapeutic proporties properties imipramine in the treatment of depression. TRH itself exerts a rapid, though brief, antidepressant effect in man and enhances l-DOPA activity in mouse. Such effects seem to be independent of thyroid hormone release by TSH. Lithium induces goitre and/or hypothyroidism in dysthymic, long-term treated patients. These effects are mediated by the strong Li+-affinity for thyroid gland, by a decrease in thyroglobulin iodination and by a reduced release of thyroid hormones. Some authors reported that lithium affects CA turnover in brain, but such results were not confirmed by others. C cells in various classes of vertebrates are grouped in ultimobranchial gland (UBG), while in most mammals they are imbedded in thyroid gland. C cells belong to the APUD cell group, a group of endocrine cells of ectodermal origin, scattered in various organs, whose common property is the production of polypeptide hormones. C cells are argentaffin for the presence of DA in their typical organelles, the dense cytoplasmic granules (DCG). In some animal species, C cells contain 5-HT instead of DA. UBG is innervated by vagal and sympathetic fibers, whose endings are cholinergic and noradrenergic. Some unmyelinated nerve fibers enter into intimate contact with a small aliquot of UBG cells and end synaptically on them. C cells produce calcitonin, an hormone stored in DCG which regulates the level of calcium in blood. Hypercalcemia causes a progressive degranulation and both calcitonin and DA are found in large amounts in the cytoplasm of C cells. l-amino I-amino acid decarboxylase and MAO were demonstrated in C cells. At present, we do not know whether C cells contain or not other enzymes of CA metabolism. Magnesium deficiency is associated with hypertrophy, hyperplasia, ultrastructural and histochemical alterations of C cells. Generally, these changes are ascribed to concomitant hypercalcemia but some data suggest that they are caused directly by magnesium deficiency. Thryroid hormones have some important metabolic effects on brain development immediately after birth. These effects become insignificant in adult individuals. On the contrary, their influence on CA metabolism clearly persists after the end of development period.

Interazioni fra ormoni tiroidei, cellule C e sistemi catecolaminici / G. Campanella, M. Popoli, A. Di Lauro, O. Silvestri. - In: ACTA NEUROLOGICA. - ISSN 0001-6276. - 32:4(1977), pp. 491-519.

Interazioni fra ormoni tiroidei, cellule C e sistemi catecolaminici

M. Popoli
Secondo
;
1977

Abstract

The literature on interrelationships among thyroid, C cells and catecholaminergic systems in the brain is reviewed. The main available data can be summarized as follows. Monoamines and their precursors (l-DOPA, DA, NA, A, 5-HT) are stimulatory to iodine incorporation and iodothyronine synthesis in the calf thyroid. DA and NA concentrations in anterior hypothalamus influence TSH secretion from hypophysis and TRH secretion from hypothalamus. Thyroxine increases NA and DA turnover in mouse brain and subsequently it increases CA receptor sensitivity. Such effects are more evident for DA than NA. Chorea occurs in a small percentage of patients with hyperthyroidism. Klawans suggested that in man hyperthyroidism increases the sensitivity of striatal receptor sites to DA. Analogously, apomorphine induces stereotyped behavior in hyperthyroid guinea pigs. CSF HVA is reduced also in patients with hyperthyroid and without chorea. L-triiodothyronine and TSH enhance the therapeutic proporties properties imipramine in the treatment of depression. TRH itself exerts a rapid, though brief, antidepressant effect in man and enhances l-DOPA activity in mouse. Such effects seem to be independent of thyroid hormone release by TSH. Lithium induces goitre and/or hypothyroidism in dysthymic, long-term treated patients. These effects are mediated by the strong Li+-affinity for thyroid gland, by a decrease in thyroglobulin iodination and by a reduced release of thyroid hormones. Some authors reported that lithium affects CA turnover in brain, but such results were not confirmed by others. C cells in various classes of vertebrates are grouped in ultimobranchial gland (UBG), while in most mammals they are imbedded in thyroid gland. C cells belong to the APUD cell group, a group of endocrine cells of ectodermal origin, scattered in various organs, whose common property is the production of polypeptide hormones. C cells are argentaffin for the presence of DA in their typical organelles, the dense cytoplasmic granules (DCG). In some animal species, C cells contain 5-HT instead of DA. UBG is innervated by vagal and sympathetic fibers, whose endings are cholinergic and noradrenergic. Some unmyelinated nerve fibers enter into intimate contact with a small aliquot of UBG cells and end synaptically on them. C cells produce calcitonin, an hormone stored in DCG which regulates the level of calcium in blood. Hypercalcemia causes a progressive degranulation and both calcitonin and DA are found in large amounts in the cytoplasm of C cells. l-amino I-amino acid decarboxylase and MAO were demonstrated in C cells. At present, we do not know whether C cells contain or not other enzymes of CA metabolism. Magnesium deficiency is associated with hypertrophy, hyperplasia, ultrastructural and histochemical alterations of C cells. Generally, these changes are ascribed to concomitant hypercalcemia but some data suggest that they are caused directly by magnesium deficiency. Thryroid hormones have some important metabolic effects on brain development immediately after birth. These effects become insignificant in adult individuals. On the contrary, their influence on CA metabolism clearly persists after the end of development period.
Settore BIO/14 - Farmacologia
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2434/177875
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