The parabrachial nucleus (PBN) has long been recognized as a sensory relay receiving an array of interoceptive and exteroceptive inputs relevant to taste and ingestive behavior, pain, and multiple aspects of autonomic control, including respiration, blood pressure, water balance, and thermoregulation. Outputs are known to be similarly widespread and complex. How sensory information is handled in PBN and used to inform different outputs to maintain homeostasis and promote survival is only now being elucidated. With a focus on taste and ingestive behaviors, pain, and thermoregulation, this review is intended to provide a context for analysis of PBN circuits involved in aversion and avoidance, and consider how information of various modalities, interoceptive and exteroceptive, is processed within PBN and transmitted to distinct targets to signal challenge, and to engage appropriate behavioral and physiological responses to maintain homeostasis.

Recent research and theory point to the possibility that hippocampal-dependent learning and memory mechanisms translate neurohormonal signals of energy balance into adaptive behavioral outcomes involved with the inhibition of food intake. The present paper summarizes these findings and ideas and considers the hypothesis that excessive caloric intake and obesity may be produced by dietary and other factors that are known to alter hippocampal functioning.Keywords energy homeostasis; memory; associative learning; obesity; rat Much research has been devoted to identifying and understanding the role of inhibitory gutbrain signals in the control of energy intake and body weight [1]. A widely-held view is that the arrival of nutrients in the gut gives rise to relatively short-term hormonal (e.g., cholecystokinin (CCK)) meal-termination or "satiety" signals [2]. The effectiveness of these signals is thought to be modulated by circulating adiposity hormones (e.g., leptin and insulin) which provide information about the longer-term, as opposed to meal-related, status of bodily energy stores [3]. In addition, ghrelin has been identified as a gastric peptide that functions as a physiological meal initiation or "hunger" cue [4] that is elicited not only as a result of a change in an animal's nutrient status but also as a learned anticipatory response to environmental cues associated with food [5]. Peripherally administered CCK and leptin appear to have interoceptive sensory consequences similar to those produced by a low level (e.g., 1 hr) of food deprivation [6], whereas the cue properties of peripherally or centrally administered ghrelin are similar to higher (e.g., 23-hr) levels of food deprivation [7,8]. All of these signals are transmitted to the brain where they are thought to be detected primarily by hypothalamic and hindbrain nuclei [2,9].While the identification of physiological meal-related and adiposity signals has contributed much to our understanding of the control of food intake and body weight regulation, relatively little is known about how the information provided by these cues is translated by the brain into adaptive behavioral outcomes. Although the hypothalamus and hindbrain have been identified Please correspond with:

Gustatory cortex (GC), an assemblage of taste-responsive neurons in insular cortex, is widely regarded as integral to conditioned taste aversion (CTA) retention, a link that has been primarily established using lesion approaches in rats. In contrast to this prevailing view, we found that even the most complete bilateral damage to GC produced by ibotenic acid was insufficient to disrupt postsurgical expression of a presurgical CTA; nor were such lesions sufficient to disrupt postsurgical acquisition and initial expression of a second CTA. However, some rats with lesions were significantly impaired on these tests. Further examination of all conditioned rats with lesions, regardless of the lesion topography, revealed a significant positive association between damage in the posterior portion of GC and especially within adjacent posterior regions of insular cortex. Accordingly, we developed a high-resolution lesion-mapping program that permitted the overlay of the individual lesion maps from rats with CTA impairments to produce a groupwise aggregate lesion map. Comparison of this map with one derived from the unimpaired counterparts indicated a specific lesion "hot spot" associated with CTA deficits that included the most posterior end of GC and overlying granular layer and encompassed an area provisionally referred to in the literature as visceral cortex. Thus, the detailed mapping of the lesion in behaviorally defined subgroups of rats allowed us to exploit the variability in performance to uncloak an important potential component of the functional topography of insular cortex; such an approach could have general applicability to other brain structure-function endeavors as well. W ith its primary receptors situated at the front end of the alimentary tract, the gustatory system is integrally involved in guiding food selection, promoting and discouraging intake, and evoking preparatory physiological reflexes (1). To best serve these functions, taste signals must confer with both the contemporary physiological milieu (e.g., satiety, malaise) and neurally stored representations of the associated effects of that particular taste stimulus [e.g., associative history with visceral malaise, as in conditioned taste aversion (CTA)]. However, the neural circuits underlying these critical integrative processes remain to be fully elucidated. In this regard, gustatory cortex (GC), an assemblage of taste-responsive neurons in the anterior dysgranular and agranular layers of insular cortex, is of particular interest (2-7). Receiving convergent input from both the thalamic and limbic taste pathways, GC consists of neurons that may potentially respond to various features of the taste stimulus, including chemosensory and hedonic alike, situated in close proximity to one another (5,(8)(9)(10)(11)(12)(13). Additionally, viscerosensory signals are received in the adjoining region of granular insular cortex (GI) just dorsal and posterior to GC (5,6,11,14). Extensive and reciprocating projections are found both within the subdivisions of G...

The gustatory system serves as a critical line of defense against ingesting harmful substances. Technological advances have fostered the characterization of peripheral receptors and have created opportunities for more selective manipulations of the nervous system, yet the neurobiological mechanisms underlying taste-based avoidance and aversion remain poorly understood. One conceptual obstacle stems from a lack of recognition that taste signals subserve several behavioral and physiological functions which likely engage partially segregated neural circuits. Moreover, although the gustatory system evolved to respond expediently to broad classes of biologically relevant chemicals, innate repertoires are often not in register with the actual consequences of a food. The mammalian brain exhibits tremendous flexibility; responses to taste can be modified in a specific manner according to bodily needs and the learned consequences of ingestion. Therefore, experimental strategies that distinguish between the functional properties of various taste-guided behaviors and link them to specific neural circuits need to be applied. Given the close relationship between the gustatory and visceroceptive systems, a full reckoning of the neural architecture of bad taste requires an understanding of how these respective sensory signals are integrated in the brain.