Pathways by Which Traumatic Stress and Ether Induce Increased ACTH Release in the Rat1

Abstract

Removal of all forebrain anterior to the superior colliculus, but leaving an intact isolated median eminence, stalk and pituitary, permits a rise in adrenocortical secretion in response to ether anesthesia, with or without additional traumatic stress, equal to that of intact controls. However, if Nembutal anesthesia is used, traumatic stress does not induce a rise in adrenocortical secretion unless a large “peninsula” is left connecting the hypothalamus to the dorsal mesencephalon and remaining hindbrain. A similar prevention of the rise in adrenal secretion occurs if leg break is produced distal to a section of the spinal cord in otherwise intact animals, but only if Nembutal and not ether anesthesia is used. It is concluded that ether apparently directly stimulates the median eminence to cause increased ACTH release. Traumatic stress induces ACTH release through ascending neural pathways feeding to the hypothalamus through the dorsal mesencephalon. (Endocrinology74: 981, 1964)