Since 1896, when blagnus-Levy suggested that the thyroid hormone might act either directly on tissues or indirectly by way of the nervous system, numerous attempts have been made to locate its site and manner of action. The opinion now, perhaps, most widely held favors a direct action upon individual cells, but even in recent years action via the nervous system has received support. Krogh ('16) reported, for example, that complete denervation of the extremities eliminated much of the metabolic rise produced in frogs by desiccated thyroid, presumably due to loss of sympathetic activity; and Abderhalden and Wertheimer ( '26) interpret the inhibitory effect of ergotamine upon the action of thyroxine as further evidence that the latter acts via the sympathetic. Most styiking are the claims of Mansfeld and Horvath ( ' 3 5 ) that the respiration of slices of kidneys from thyroxinized dogs is not increased above normal when the kidney has been denervated before hyperthyroidism was induced, and that the respiration of the frog gastrocnemius is increased a third when only the cut end of its nerve is dipped for some hours in Ringer containing thyroxin. These findings were interpreted to mean that the hormone is carried to parenchymal cells only along efferent nerve fibers.
Whatever additional role the nervous system plays in raising basal metabolism-by increased motor discharges to smooth