We have measured thyroid and adrenocortical function in unanesthetized stressfree rats after stimulation by cold exposure, TRF, or TSH. Initial studies suggested an inverse relationship between the 2 systems in response to cold. Dexamethasone was administered to rats prior to cold exposure to determine if suppression of ACTH would alter the response of the hypothalamo—pituitary— thyroid axis (HPTA). 250 μg dexamethasone/ 100 g bw inhibited the HPTA response to cold but did not suppress TRF induced TSH release. Therefore this dose of steroid inhibits coldinduced TRF release. Since the cold response, but not the TRF response, was blocked by dexamethasone we also conclude that the response to acute cold is mediated via TRF release. This dose of dexamethasone actually enhanced the pituitarythyroid response to TRF. This effect is exerted at the level of the pituitary since the thyroid response to TSH was unaltered. A lower dose of dexamethasone (25 μg/100 g bw) accentuated the HPTA response to cold and since this dose of steroid did not alter the pituitary response to TRF the site of action must be above the pituitary. Rats treated with diphenylhydantoin, to prevent the suppressive effect of dexamethasone on ACTH, exhibited the same accentuation of the HPTA response to cold. Our findings indicate that various effects of dexamethasone on TSH secretion may be seen depending upon dose and time schedules employed. Furthermore, these findings can be attributed, at least in part, to direct effects of the steroid on the HPTA rather than to suppression of ACTH secretion. (Endocrinology 92: 1305, 1973)