Gustatory nucleus

(VII), the glossopharyngeal nerve (IX), and the vagus nerve (X). Taste cells synapse with primary sensory axons of three cranial nerves; the facial nerve, glossopharyngeal nerve, and the vagus nerve. These cranial nerves innervate the taste buds in the tongue, palate, epiglottis, and esophagus. The primary sensory neurons of these central axons are in the cranial nerve ganglia of each respective cranial nerve. To produce the sense of taste, these neurons project to the gustatory nucleus, or the rostral and lateral regions of the nucleus of the solitary tract, and are ultimately projected to the cerebral cortex. Topography on the tongue doesn't determine the arrangement and processing of input within this nucleus. Instead, individual gustatory nuclei processing information is influenced by separate taste bud populations. Some examples of gustatory cranial nerves, that innervate the taste buds and are connected to this nucleus include the chorda tympani and lingual branch of the glossopharyngeal nerves. Tastants are the chemical molecules that provide the stimulus for taste perception. The concentration of this taste stimulus is what dictates the intensity of the taste sensation that is perceived. Furthermore, the threshold concentration for a required degree of sensation varies depending on the specific tastant. However, in general, threshold concentrations for tastants are very high relative to other sensory stimuli such as odorants. == Gustatory nucleus and obesity ==

Numerous studies have investigated the connection between the gustatory nucleus and obesity; an increase in visceral fat is negatively correlated with taste function. In both humans and rats, taste sensitivity changes with body weight, especially sweet and fat taste qualities that signal high energy availability. The nucleus tractus solitarii (NTS), which includes the gustatory nucleus, has neurons that express many different receptors that inform organisms of their internal state and are involved in the homeostatic regulation of ingestion. This shows the role of taste as a sensory regulator of food consumption that produces different responses depending on the chemical composition of a food. However, in rats and humans with obesity, there is a reduction in taste receptor cell expression as well as reduced activation of taste receptor cells. In one study, the effect of obesity on responses to taste stimuli in the NTS was investigated by recording taste responses from single cells in this sensory region of rats with diet induced obesity due to a high energy diet and lean rats fed a normal diet. Results of the study showed that rats with diet induced obesity produce a more prevalent response to taste in the gustatory nucleus of the NTS as well as a weakened association between taste responses and ingestive behavior compared to lean rats. In addition, it was also discovered that the responses to taste stimuli in rats with obesity were smaller, shorter, and occur at longer latencies compared to those of lean rats. These electrophysiological recordings create a connection between the gustatory nucleus and obesity as exposure to a high energy diet can alter how taste is encoded by the nervous system. In both humans and rats with obesity, taste responses are shorter and weaker and can have a large impact on how the brainstem represents taste stimuli. This ultimately effects food choice and body weight, resulting in a possible increase in consumption of high energy foods, such as sugars and fats. ==References==