Evidence of Central Nervous System Influence Upon Cold-Induced Acceleration of Thyroidal I131 Release

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Abstract
During the initial 12 hours of cold-exposure (5°C) of the hamster, thyroidal I131 release is accelerated markedly. Bilateral nephrectomy, adrenal demedullectomy or adrenalectomy do not influence this response. Treatment of animals with reserpine, placement of appropriate median eminence lesions 24 hours before exposure, or chronic lesions (3–6 weeks) do not interfere with subsequent normal hormone delivery but do block the accelerated release attendant upon cold exposure. Using hypophysectomized hamsters, I131 uptake is restored to normal by treatment with TSH. After this uptake is achieved and exogenous TSH discontinued, release from the thyroid is slow and cannot be accelerated by cold. Transplantation of fragments of 1/2–2 pituitary glands into the cheek pouch of hypophysectomized hamsters temporarily restores both uptake and release. Cold-exposure, however, does not accelerate thyroidal release in such graft-bearing animals. These experiments indicate that upon cold-exposure a central nervous system stimulus is responsible for triggering the pituitary-thyroid system and that the accelerated thyroidal I131 delivery, depending upon increased secretion of TSH, requires adenohypophyseal tissue with its normal anatomical connections to the hypothalamus.