Chemotherapy-induced XXXX intake is increased by lesion of the lateral parabrachial nucleus of the @entity35 .

@entity390 @entity10789 @entity19 @entity4563 @entity391 @entity900 @entity5019 @entity3826 @entity4326 @entity35
Anticancer agents, such as @entity900 , stimulate @entity390 , @entity391 , and behaviors indicative of malaise. @entity35 and @entity19 do not possess a @entity391 response, and, therefore, in these species, the ingestion of @entity4563 clay (a pica response) has been used as an index of malaise. In the @entity35 , @entity900 -induced @entity4563 intake is inhibited by antiemetic treatments. In addition, @entity900 activates vagal afferent fibers in the gut, and @entity4563 intake induced by @entity900 is largely dependent on an intact vagus. Nevertheless, little is known about the brain pathways controlling pica. We investigated the role of the lateral parabrachial nucleus (lPBN), a major visceral afferent link between the hindbrain and forebrain, in @entity900 -induced @entity5019 expression and pica. Injection of @entity900 (6 mg/kg ip) produced @entity5019 expression in the @entity10789 , a region receiving viscerosensory input. In @entity35 with bilateral @entity4326 lPBN lesions, @entity900 treatment substantially increased @entity4563 intake compared with controls ( approximately 30 g vs. approximately 5 g, respectively, over 24 h). Food intake was reduced by @entity900 treatment and by @entity3826 , an emetic agent that acts centrally. Unlike @entity900 , however, @entity3826 stimulated @entity4563 intake to a similar degree in both the lesioned and control @entity35 , suggesting that lPBN damage neither produces nonspecific effects nor enhances malaise in general. These data suggest that lPBN-lesioned animals not only demonstrate pica after @entity900 treatment, but, in fact, show an exaggerated response that is greatly in excess of any treatment known to produce @entity4563 intake in @entity35 .
