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The body weights of male albino rats were reduced gradually to 80% of normal body weight by restricting food intake (dieting), and then the rats were given lateral hypothalamic (LH) lesions. Compared with rats of normal body weight sustaining similar brain lesions, the dieted group displayed a shorter period of postoperative aphagia and less gastric pathology. In a second experiment, a group of rats was reduced to 80% of normal body weight by withholding all food (fasting) and then given LH lesions. Compared with dieted rats sustaining similar brain damage, the fasted group displayed a longer period of postoperative aphagia and greater gastric pathology. Since the duration of aphagia could be shortened or lengthened by simple manipulations of preoperative body weight, the adequacy of sensorimotor or motivational hypotheses to account for aphagia is questioned. The results are more consistent with the suggestion that gastric abnormalities produced by LH lesions inhibit eating. This research was supported by Grant MRan( j the orientation to somatic and olfactory w 13 ^^ K the N , at . ional Institute of Mental ^^^j ( Marsha n & Teitelbaum, 1974; Health and by an Arizona State University Fac-,, , " ^ e ^ -x iu im-i ulty Grant-In-Aid Award to Ernest Lindholm. Marshall, Turner, & Teitelbaum, 1971; Experiment 1 was the master's thesis of Carlos Turner, 1973). These dysfunctions have Grijalva, who was supported by a Ford Founda-been referred to as sensory neglect (Marshall tion Graduate Fellowship. The authors thank J. e t & \ 1971), sensory inattention (Marshall J %™ t f 7 helpfUl t Cri l iCiS M S K ** if * & Teitelbaum, 1974), or the sensorimotor Requests for reprints should be sent to Ernest , /m ' ,«""•> CT --i

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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.