Nutrition is one of the most important components to a long, healthy life. This evidence is not only common sense; the fact is constantly circulating in the media as well as in commercials and various other types of advertisement. In today's modern society the ability to taste and distinguish between foods is usually only brought to light when deciding which brand of potato chips to buy from the store or picking between two of your favorite dishes at a restaurant. However before the Food and Drug Administration was formed to protect people from harmful substances in food, human's only defense against poison besides prior knowledge from personal experience or through the teachings of others, was by aid of their tongues.
The ability to taste is closely related to the olfactory tract -the sense of smell- in both functionality and hierarchy structures in the brain. The purpose of this paper will be to cover an in depth exploration of the neocortical areas associated with taste and how these areas are organized. The four primary taste modalities we associate with taste in Western cultures ( sweet, salty, bitter, and sour) will also be explored by discussing their distinctive spatial patterns in the brain; the fifth modality the taste of glutamate, termed umami- will also be covered (Accolla, R., Bathelier, B., Peterson, C., H., & Carleton, A., 2007).
This paper will also explore the neuromodulatory systems and neurotransmitters involved in the long-term encoding of new tastes and unfamiliar tastes in rats. In rats, the admission of a novel taste activates the extracellular signal-regulated kinase 1-2 (ERIK1-2) in the insular cortex which is a part of the taste pathway (Berman, D., Hazvi, S., Neduva, V., & Dudai, Y., 2000).
Finally, diseases and disorders that affect the gustatory cortex and the taste pathways will be discussed. (Campbell, N., Reece, J., Urry, L., & Cain, M. L, 2008).
Chemoreceptors govern the perception of both gestation and olfaction (taste and smell). It is not surprising then to note that taste and smell are closely correlated. For example, amphibians exhibit no distinction from gustatory or olfactory stimulation. The chemicals that are detected by the gustatory cortex are called tastants. In mammals the receptor cells that govern taste are not neurons as is the case in olfaction; rather they are modified epithelial cells organized into papillae or taste buds. Taste buds on any region of the tongue can detect any of the taste modalities (sweet, salty, bitter, sour and umami). Receptor proteins for all of the taste modalities have been identified, with the exception of salty. Sweet, bitter, and umami taste modalities require a metabotrophic receptor channel through a G protein-coupled receptor. Only the sour modality which resembles thermoreceptor proteins such as capsaicin receptors use ionotrophic channels. In the case of the sour modality when an acid or sour tasting substance build up, the action potential builds until the threshold is reached and depolarization of the membrane causes the Na+ channels to open. Only one receptor has been identified for both sweet and umami modalities. However over 30 receptors have been identified for bitter tastes. This observation is not coincidental. From an evolutionary stand point it would make sense that more receptors would be attributed to bitter tastes. Poison is often a bitter substance and obviously harmful if not fatal. Mammals thus have an advantage when consuming tastants in the wild. It would be more beneficial to the prolonging of the animals' race if the organism were more attuned to harmful substances (Campbell, N., Reece, J., Urry, L., & Cain, M. L.(2008).
The chemical information that is detected by the chemoreceptors becomes encoded into the perception of taste. This information extends down the taste pathway to the Gustatory Cortex. The Gustatory Cortex is located in the insular cortex anterior to the posterior parts that receive visceral inputs; the anterior insula projects to the amygdala. It also includes the frontal operculum; the primary taste cortex or gustatory cortex in often abbreviated AI/FO. In a 2007 study involving rats, tastant solutions were applied to the tongue. The tastants consistently activated regions of the Gustatory Cortex. Conducted invivo, red dye was injected into the regions of the tongue that the taste signals were observed. The same red dye was found in the Gustatory Cortex after the rat's brains were processed. This verified that the signals did indeed go to the Gustatory Cortex. Functional spatial patterns lead to the indication that differences in the fundamental neural representations were different for the taste modalities at the cortical level. Bitter and sweet modalities were represented caudally in the gustatory cortex (Accolla, R., Bathelier, B., Peterson, C., H., & Carleton, A., 2007).
In rodents the palatability of a tastant takes place in the centers of the lower brainstem, the parabrachial nucleus of the pons and the nucleus of the solitary tract in the medulla. The invivo optical imaging found that tastants activated spatial areas in the Gustatory Cortex in rats that were specific to each taste modality and essential for normal taste discrimination. This has proposed a possible way for the Gustatory Cortex to keep track of tastants in memory.
Since the anterior insula projects to the amygdala and this is where the gustatory cortex is located, the correlation between the amygdala is assumed. The amygdala controls emotional behavior, it is also an important component in memory retention. This link between brain areas may be part of the reason that taste memory and aversion are sensitive to small variations in tastants (Bender, G., Veldhuizen, M., Meltzer, J., & Gitelman, D., 2009).
In another study involving rats the consumption of a novel taste activated the extracelleular signal-regulated kinase 1-2 (ERIK1-2). A familiar taste did not activate this receptor. Activation of ERIK1-2 proved to be necessary for the encoding of long-term memories of novel tastes but not short-term memories. NMDA receptors, metabotropic glutamate receptors, and dopaminergic receptors were all contributors to the development of new novel taste memories but did not aid in retrieval. The study revealed that only the NMDA and dopaminergic receptors mediated the taste-dependent activation of ERIK1-2 specifically. This study reveals the complexity of various neurotransmitters in the gustatory cortex (Berman, D., Hazvi, S., Neduva, V., & Dudai, Y., 2000).
Nerve damage and diseases can affect the sensory input of taste, thus disrupting gustatory functioning. Ageusia is the complete loss of taste. It is characterized by an inability to distinguish the five taste modalities (sweet, sour, bitter, salty, and umamai). The causes of ageusia can include damage to the nerves that support the tongue. The lingual nerve relays sensory information from the anterior most part of the tongue, roughly 2/3s. The glossopharyngeal nerve serves the same function except with the posterior 1/3 of the tongue. Endocrine disorders can also cause taste loss. Deficiencies of certain vitamins such as Niacin and Zinc disrupt endocrine functions which affects taste loss. Certain drugs used to combat rheumatoid arthritis have also been documented to effect the gustatory complex and the sense of taste (Campbell, N., Reece, J., Urry, L., & Cain, M. L., 2008).
Dysgeusia is a more common disease of the gustatory cortex. The symptoms are not a complete lack of the sense of taste as in ageusia, but rather a distortion of normal gustatory function. Two causes are most documented in cases of dyspepsia: chemotherapy and zinc deficiency. Chemotherapy typically causes damage to the salivary tissues as well as the oral cavity. This damage makes the papillae on the taste buds harder to transmit signals to the gustatory cortex. Artificial saliva and zinc supplements have been shown to reverse dyspepsia (Campbell, N., Reece, J., Urry, L., & Cain, M. L., 2008).
