Influence of the Nursing Stimulus Upon Thyroid Hormone Secretion in the Lactating Rat

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Abstract
The influence of the nursing stimulus upon thyroid gland secretion was tested in the lactating rat during mid-lactation. Milk removal from the 6 pectoral mammary glands was prevented in all rats by galactophore ligation on postpartum day 2. Injection of 1.5 μg/100 g/day L-thyroxin was less effective in blocking thyroidal 131I release in lactating rats than in nonlactating rats. The effectiveness of the injected thyroxin in the lactating rat increased within 24 hr after the young were removed. In another experiment, a significant increase in plasma PB131I resulted from 6 hr of normal nursing of the pelvic mammary glands. No increase in plasma PB131I occurred following 6 hr of nursing of pelvic mammary glands from which milk removal was prevented by ligation of the galactophores. When the pelvic mammary glands were deprived of somatic sensory innervation by spinal cord transection and the contained milk was removed by nursing young with the aid of oxytocin injections to the mothers, the PB13lI level after 6 hr increased significantly and was comparable with that following normal nursing. Neither nursing of similar glands without oxytocin, and hence without milk removal, nor injecting oxytocin into rats non-nursed during the same period of time altered the plasma PB13lI levels. No detectable increase in PB131I occurred when only part of the milk was removed from intact normal pelvic mammary glands. The nursing-induced increase in PB131I was blocked with exogenous thyroxin and the PB131I was elevated in non-nursed lactating rats following injections of thyrotrophin. These data suggest that the nursing stimulus elevates thyroid secretion in the lactating rat as the result of the effects of milk removal and/or milk reaccumulation by the mammary gland rather than as the result of excitation of neural receptors in the nipple or skin overlying the mammary glands. The data also suggest that the effect on the thyroid gland is mediated by adenohypophysial thyrotrophin. (Endocrinology75: 15, 1964)