Signals from the mouth and gut interact in the central nervous system to regulate ingestion. In the mouth, taste stimulation initially influences the decision to ingest and also promotes ongoing ingestion. In the gut, chemoreceptors and mechanoreceptors signal satiety, and thus help to suppress further intake. Behavioral studies show that ingestion is characterized by an inhibitory influence derived from an accumulating post-ingestive load that progressively counters the excitatory influence of taste on promoting ingestion. Mechanisms of this taste-visceral afferent integration are largely unknown, but likely involve neural signals reaching specific ventral nervous system loci, including the parabrachial nucleus (PBN), a site that receives strong convergent projects from second order taste and visceral afferents. The present series of experiments will test the hypothesis that the PBN is an important site for food intake regulation by determining (1) whether gastric and intestinal mechanoreceptor signals converge upon and modulate taste-sensitive neurons in the PBN, and (2) whether metabolic/nutrient-related signals from the liver and duodenum also influence taste-sensitive neurons in the PBN. Eating, metabolic and gastrointestinal disorders contribute to numerous diseases including hypertension, stroke and diabetes. An understanding of where and how taste and visceral signals are processed in the brain is fundamental to developing clinical interventions.
| Hu, Zhengqing; Ulfendahl, Mats; Prieskorn, Diane M et al. (2009) Functional evaluation of a cell replacement therapy in the inner ear. Otol Neurotol 30:551-8 |
