NEURAL CONTROL OF ACTH RELEASE IN RESPONSE TO HEMORRHAGE

Publisher Website
Google Scholar
Abstract
A three dimensional reconstruction of the central neural pathways that appear to mediate release of ACTH in response to hemodynamic change is illustrated in Figure 11. Fibers from receptors in the right atrium and the carotid arteries project to the lateral solitary nucleus and then to the medial and the lateral nucleus intercalatus. A pathway containing projections from these nuclei then converges dominantly in the locus subcoeruleus and locus coeruleus. Multiple pathways then diverge, to travel in part directly to the hypothalamus through dorsal pathways. One pathway inhibits and another facilitates the release of ACTH. Multiple pathways also diverge, to travel in part medially, and then to the hypothalamus through ventral pathways. Again, one pathway inhibits and another facilitates the release of ACTH. The dorsal and ventral inhibitory pathways appear to converge in a region extending from just caudal and ventral to the paraventicular nucleus to the posterior hypothalamic area. Thus, after the coalescences of the various pontine-hypothalamic pathways, three principal pathways remain. These include a posterior inhibitor path, an anterodorsal facilitatory path that terminates in the paraventricular nucleus and that may be mediated through release of vasopressin, and an anteroventral facilitatory path that terminates in the suprachiasmatic and ventromedial nuclei and that is probably mediated through release of corticotropin-releasing hormone. The mode of integration of these pathways has not been defined. The pathways described herein are oligosynaptic: a signal may travel from atrium to hypothalamus over three to seven neurons. The combination of control of input hemodynamic signals and of measurement of ACTH permits quantitation of both sensory and motor events, that inevitably must be embedded in the neuronal pathways described here. The analysis of the input-output relations and their correlation with internal neural events must form the basis of a description of the physiology of the physiology of the system whose central neural anatomy has been defined in part by these studies.