Necessity of the glossopharyngeal nerve in the maintenance of normal intake and ingestive bout size of corn oil by rats

Recent evidence in the literature suggests that signals carried by the glossopharyngeal nerve (GL), which supplies sensory and parasympathetic innervation of the posterior tongue, might be essential in the maintenance of normal gustatory responses to fat stimuli. Here, we report that GL transection (GLX) significantly decreased corn oil intake and preference in 23-h two-bottle tests relative to sham-operated controls (Sham). Drinking-pattern analysis of corn oil licking revealed that bout size, rather than the number of bouts initiated, was smaller in GLX than Sham rats. We also tested a range of glucose concentrations and found that total licks over daily 23-h sessions significantly decreased in GLX compared with Sham rats, but this difference failed to reach significance when intake or any bout parameter was measured. These results show that the signals in the GL normally contribute to processes involved with corn oil bout termination as opposed to bout initiation. GL-derived signals could potentially provide input to “reward” circuits in the ventral forebrain that could serve to maintain ingestion during a meal or, alternatively, could act at the level of the brain stem to attenuate the inhibitory potency of vagal signals, thus delaying the onset of satiation, or perhaps contribute to a cephalic phase reflex modulation of the gut. Parasympathetic efferents in the GL innervating the von Ebner's glands, which secrete lingual lipase, which is thought to break down corn oil into detectable ligands, could also be playing a role in driving corn oil intake. Whatever the mechanism, an intact GL is clearly necessary in maintaining normal intake of corn oil

The taste of table salt

Solutions of table salt (NaCl) elicit several tastes, including of course saltiness but also sweet, sour, and bitter. This brief review touches on some of the mileposts concerning what is known about taste transduction for the Na(+) ion, the main contributor to saltiness. Electrophysiological recordings, initially from single gustatory nerve fibers, and later, integrated impulse activity from gustatory nerves led researchers to predict that Na(+) ions interacted with a surface molecule. Subsequent studies have resolved that this molecule is likely to be an epithelial sodium channel, ENaC. Other Na(+) transduction mechanisms are also present in taste buds but have not yet been identified. The specific type(s) of taste cells responsible for salt taste also remains unknown