Injections of 2-deoxyglucose into the hepatic-portal system of normal rabbits increased eating to a greater extent and with shorter latency than comparable injections of 2-deoxyglucose into the jugular vein or into the hepaticportal circulation of the vagotomized rabbit. These differences suggest the existence of vagally mediated peripheral glucoreceptors important in the initiation of food intake.
Hypertonic saline and sucrose, but not urea, induced drinking when injected (2 /A. in 1 min.) directly into the lateral preoptic area (LPO) near the anterior commissure. In contrast, local cellular dehydration was not a stimulus in the dorsal (DHA) and lateral hypothalamus (LHA) where hypertonic saline nonspecifically excited neurons to induce drinking or eating. Rabbits allowed isotonic saline and water chose water immediately following either intravenous injections of hypertonic saline or intracranial injections into LPO, but not following injections into DHA or LHA. Electrolytic lesions, including the osmosensitive portion of LPO, abolished the drinking that normally follows intravenous injections of hypertonic saline although ad-lib water intake was normal and not dependent upon the intake of dry food.1 A preliminary account of these experiments was given by D.
A foregone conclusion is that central neural and endocrine control of gastrointestinal functions is based on a complex array of interconnecting brain structures, neurochemical systems, and hormonal modulators. As might be expected, a considerable degree of redundancy is seen not only in the manner in which certain brain structures appear to participate in the regulation of GI functions, but also in the extent to which certain neurotransmitters or brain-gut peptides, when injected centrally, alter these functions. Despite the seemingly ambiguous nature of brain-gut interactions, a picture is beginning to unfold that suggests that GI properties are based on certain reflexes (e.g., vago-vagal). These reflexes, in turn, appear to be influenced by brain structures in a hierarchical manner, not all that dissimilar to the system described by Papez and expanded on by MacLean several years ago. For example, the perceptual or cognitive aspects of both external and internal stimuli are monitored at various brain levels, but obviously higher cortical processes are intimately involved. Aversive events provide sensory information, which is integrated primarily by the limbic system (e.g., amygdala) and translated into the expression of emotional behavior and associated autonomic response patterns. Various hypothalamic structures, in turn, appear most strongly to influence physiological changes associated with aversive events by virtue of the direct connections to the autonomic and endocrine systems. Ultimately, the visceral outcome can be seen as being based on the integrated convergence of information from cortical, limbic, and hypothalamic structures onto medullary nerve nuclei as well as other efferent systems. With respect to animal models of neurogenic or stress ulcer, activity of the dorsal vagal complex and vagal efferents appears to be the final common pathway for pathologic changes in the gut.
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