Experiments were performed to delineate the afferent pathways through which traumatic stress reaches the basal hypothalamus. ACTH secretion in response to a unilateral leg break or a tight rubber band around the tibia was assessed by a rise in plasma corticosterone 20 min later. Complete basal hypothalamic deafferentation blocked the rise in plasma corticosterone caused by a leg break on either side. Unilateral basal hypothalamic deafferentation significantly blocked contralateral but not ipsilateral leg break. Contralateral leg break was not blocked if a 1 mm rim of tissue was left below the unilateral deafferentation. Contralateral leg break was also blocked by an anterior quarter section on one side but not by a posterior quarter section. Neither unilateral nor complete basal hypothalamic deafferentation blocked the rise in plasma corticosterone following a rubber band tourniquet on a single extremity. In all operated groups with “effective” deafferentations, including complete basal hypothalamic isolation, about half the rats had a variable increase in plasma corticosterone following leg break. This may have been due to non-neural components for ACTH release or incomplete deafferentation in those animals. It is concluded that the pathway via which a single leg break causes increased ACTH secretion is usually contralaterally distributed at the level of the basal hypothalamus as well as through the spinal cord to the pons. This pathway enters the anterior basal hypothalamus within 1 mm of the ventral brain surface. A rubber band tourniquet probably increases ACTH secretion through some pathway different from that followed by the stimulus of a leg break. (Endocrinology86: 1404, 1970)
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Greer et al. (1970) studied this question.