L. E. Ericson

Fluorescence and electron microscopy of amine-storing enterochromaffin-like cells in tracheal epithelium of mouse.

SummaryThe tracheo-bronchial mucosa of the mouse has been found to contain an extensive system of argyrophilic epithelial cells. In the trachea the cells morphologically resemble enterochromaffin cells. Normally, these enterochromaffin-like cells contain no fluorogenic amine, as revealed by the Falck-Hillarp formaldehyde technique. On the other hand the cells have the capacity to take up and decarboxylate 3,4-dihydroxyphenylalanine (DOPA) or 5-hydroxytryptophan (5-HTP); the amine formed is stored in the cytoplasm in a reserpine-sensitive store. This capacity to produce and store amines under experimental conditions may reflect the presence in the tracheal enterochromaffin-like cells of an amine which can not be demonstrated with available fluorescence histochemical techniques. In the electron microscope the tracheal enterochromaffin-like cells were identified by a positive argyrophil reaction and by their capacity to accumulate radioactivity after administration of 3H-DOPA or 3H-5-HTP as revealed by autoradiography. The radioactive labelling was associated with cytoplasmic electron-dense granules (800–1000 Å), suggesting that the amine formed was stored in these granules. Accordingly, the granules stained argentaffin after DOPA-pre-treatment of the animal. It is suggested that, like similar cells in the gastric mucosa, these argyrophilic enterochromaffin-like cells constitute an endocrine system in which amines are of cytophysiological importance.

Intracellular distribution of amines and calcitonin in the sheep thyroid gland

The distribution of amines (dopamine, histamine, 5-hydroxytryptamine, and norepinephrine) and calcitonin in the sheep thyroid gland was studied by quantitative analyses of these substances in subcellular fractions examined with the electron microscope. The fractions were prepared by centrifugation in continuous sucrose gradients. Histamine was mainly found in the supernatant fraction and dopamine in the gradient pellet together with mast cell granules. This indicates a release of histamine, but not of dopamine, from the mast cell granules, which contain both these amines. Norepinephrine was mainly recovered in the supernatant fraction and adjacent fraction. 5-Hydroxytryptamine and calcitonin were concentrated in one fraction. This fraction contained a high concentration of dense, argentaffin granules, indistinguishable from those found in sections of parafollicular cells. These observations show that 5-hydroxytryptamine and the polypeptide calcitonin are both stored almost exclusively in the cytoplasmic granules of the parafollicular cells.

Sympathetic regulation of thyroid hormone secretion

Publisher Summary This chapter discusses the sympathetic regulation of thyroid hormone secretion. The finding of sympathetic nerve terminals very close to thyroid follicle cells signifies that there is a morphologic basis for a direct, nonvascular, influence of sympathetic stimuli on thyroid hormone secretion. There is also evidence that such an influence is exerted. In mice, whose TSH secretion has been eliminated, sympathetic stimulation or administration of norepinephrine (NE) or other arylmethylamines induces secretion of thyroid hormone, as reflected by signs of endocytosis of thyroglobulin followed by release of thyroidal radioiodine into the blood. The secretory response to sympathetic stimulation is restricted to the thyroid regions supplied by the stimulated nerve, indicating that the effect results from an action of NE released within the gland. The thyroid activation is probably induced by the amine as such the effect is augmented after pretreatment with a monoamine oxidase inhibitor, and the catecholamine precursor DOPA exerts a thyroid-stimulating effect only after its decarboxylation to dopamine. It is found that although catecholamines certainly affect thyroid blood flow, their stimulatory effect on the thyroid hormone secretion cannot entirely be explained by their influence on thyroid vessels, and it is rather the result of a direct action on the follicle cells.

Thyroid parafollicular cells: Ultrastructural and functional correlations

The existence of a second plasma calcium regulating hormone besides the parathyroid hormone was demonstrated in 1962 (1). The thyroid origin of this hormone, calcitonin, was rapidly established. The detection of calcitonin initiated studies in many laboratories in order to characterize its structure and its biological activities. Calcitonin is a polypeptide consisting of 32 amino acid residues. The most thoroughly studied effect of calcitonin has been its ability to lower plasma calcium concentrations by suppressing bone resorption (2).

SYMPATHETIC REGULATION OF THYROID HORMONE SECRETION

Publisher Summary This chapter discusses the sympathetic regulation of thyroid hormone secretion. The finding of sympathetic nerve terminals very close to thyroid follicle cells signifies that there is a morphologic basis for a direct, nonvascular, influence of sympathetic stimuli on thyroid hormone secretion. There is also evidence that such an influence is exerted. In mice, whose TSH secretion has been eliminated, sympathetic stimulation or administration of norepinephrine (NE) or other arylmethylamines induces secretion of thyroid hormone, as reflected by signs of endocytosis of thyroglobulin followed by release of thyroidal radioiodine into the blood. The secretory response to sympathetic stimulation is restricted to the thyroid regions supplied by the stimulated nerve, indicating that the effect results from an action of NE released within the gland. The thyroid activation is probably induced by the amine as such the effect is augmented after pretreatment with a monoamine oxidase inhibitor, and the catecholamine precursor DOPA exerts a thyroid-stimulating effect only after its decarboxylation to dopamine. It is found that although catecholamines certainly affect thyroid blood flow, their stimulatory effect on the thyroid hormone secretion cannot entirely be explained by their influence on thyroid vessels, and it is rather the result of a direct action on the follicle cells.