Neurophysiology: The Human Senses of Olfactory & Gustatory


by Robert Harwell, M.S.


This paper will describe, discuss, and evaluate the physiology and function of olfaction, abnormalities and implications of olfactory disorders, the physiology and function of gustation, and abnormalities and implications of gustatory disorders.

Physiology and Function of Olfaction

The stimulus for smell begins when airborne molecules are inhaled and pulled in and circulated through the nasal cavity, where the olfactory receptors are located. Odor-bearing vapors can also reach the nasal cavity from the mouth and past the throat through a chimney-like passage which leads to the smell receptors. While the air circulates around a series of baffles formed by three small mucous-covered bones called turbinates, it is warmed and humidified by tiny hairs lining the nasal cavity, removing any debris. In fact, for most people the left and right nasal airways work in alternating shifts called the nasal cycle. The average airflow through an engorged nostril is 31 liters of air per minute. However, the airflow through the other nostril is 51 liters per minute, a 64 % difference (Blake & Sekuler, 2006).

The receptor cells that register the presence of odorous molecules sit on the olfactory epithelium, which forms part of the ceiling of the nasal cavity and measures 1.3 centimeters in diameter. Each nasal cavity has it own olfactory epithelium, and within each olfactory epithelium are olfactory sensory neurons (OSN), bipolar nerve cells that capture odorant molecules and initiates the neural signals for smell. At one end of this nerve cell a single dendrite terminates in numerous tiny cilia. On its opposite end, the nerve cell terminates in a single axon, forming with other axons a sensory fiber that threads through the perforations in bone that form the roof of the nasal cavity. Typically, the human nose contains 40 to 50 million olfactory sensory nerves. Comparatively, a dog's nose has 10 to 20 times as many sensory nerves. Finally, there are free nerve endings that do not respond to odor sensations but do influence the perception of odors (Blake & Sekuler, 2006).

Because of their structure, OSNs simultaneously transduce chemical stimulation into neural impulses, and carry these impulses to the brain along their axons that make up the olfactory nerve. OSNs have a very short life of about five to eights weeks, and are constantly replaced when they die. A gland located in the olfactory epithelium produces a protein occurring only in the nasal tissue, and a duct carries the protein to the tip of the nose where it is mixed into the incoming air. There the protein is carried with the newly mixed air to the olfactory receptors. The receptors on the OSN cilia are long protein molecules that weave back and forth through the colliery membrane. Mammals, including humans, have up to 1,000 different receptor proteins. Each member of this family of protein receptors has three characteristics: they crisscross the membranes of the host cells seven times, use the same basic mechanisms for initiating signals, and share common characteristic sequences of amino acids. Each OSN produces only one of the possible olfactory receptor proteins (Blake & Sekuler, 2006).

The steps in the perception of an odor begin when odorant molecules bind to specific sites on the receptor protein. These binding sites are pockets created by the twists and bends of a protein as the chain folds itself into its preferred three-dimensional structure. It is the differences among amino acid strings of a protein that guarantee its structure will be unique. Because the bond of the odorant molecule is weak, it bonds to several different sites on the receptor protein. Once an odorant molecule has firmly docked with its matching receptor protein, the receptor signals a series of events in rapid succession that recruit several different chemical intermediaries within the olfactory receptor neuron. The final intermediary is an enzyme that triggers electrical changes in the cell membrane, transducing the capture of the odorant molecule to an electrical signal (Blake & Sekuler, 2006).

Finally, there is the question of why our species developed such loose dependence on a sense of smell. The answer possibly may lie with our vision system. It is speculated that the development of our full three-pigment color vision, as well as our growing reliance on it, led to a relaxed need for a sensitive sense of smell. This speculation theorizes that the relaxation of the human sense of smell shielded our species from the harsh selection pressures that would have accompanied a more sensitive sense of smell (Blake & Sekuler, 2006).

Abnormalities and Implications of Olfactory Disorders

Deficiencies in smell often go unnoticed. One cause of deficiencies in smell is a blow to the head, resulting in anosmia, commonly thought of as odor blindness. Another cause is the inhalation of caustic agents such as lead or zinc, and a third cause is Alzheimer's. These events can cause either temporary or permanent loss of smell. Temporary loss of smell may involve a restricted sense of smell. Approximately 3% of the U.S. population cannot smell sweat, 12% cannot smell musky odors, and 47% cannot smell urine. Individuals with complete anosmia often report that eating is no longer pleasurable, resulting in loss of appetite and weight and a loss of libido (Blake & Sekuler, 2006).

When tested for impairment of odor detection threshold, odor discrimination, and odor identification, Alzheimer's patients showed partial correlations. This supports prior research of olfactory dysfunctions both in patients with Alzheimer's and in those with preclinical Alzheimer's. Brain areas involved in olfactory function are situated in the medial temporal regions that undergo early pathological changes in Alzheimer's. Correspondingly, patients with Alzheimer's can expect development of olfactory dysfunctions in the early stages of the disease. Further, the progression of olfactory dysfunction correlates with the progression of Alzheimer's, as opposed to a major depression, and may be useful in differential diagnosis. This may also be useful as a diagnostic marker in predicting the incidence of Alzheimer's in high risk individuals (Peters et al., 2003).

Both anosmia and reduced sense of smell are correlated with a wide variety of neurological and psychiatric diagnoses. However, in relation to a closed head injury following either a blunt force acceleration or deceleration trauma, it is theorized that post-traumatic olfactory impairment can be a clinical sign associated with damage to the anterior regions of the brain. Current theory is that this type of head trauma results in a shearing injury at the level of the olfactory nerves as they penetrate the cribriform plate toward the olfactory bulb. A reduced sense of smell also may result following a mild or moderate traumatic brain injury (TBI). This is most often associated when the TBI causes damage to the orbital frontal cortex. TBI associated with blast exposure associated with modern warfare may also cause olfactory dysfunctions (Robert, Sheehan, Thurber & Roberts, 2010).

Physiology and Function of Gustation

The basic terrain of taste begins with the tongue, a muscle covered with a mucous membrane. Papillae arranged in regularly-spaced columns separated by channels cover the tongue, and are lined with taste buds that resemble garlic bulbs. However, not all the papillae have taste buds: those in the middle of the tongue have none. Taste sensation appears to originate from the entire surface of the mouth. Taste buds are not restricted to an individual's tongue, which contains less than 1% percent of the taste buds, but rather are found in the throat, the mouth, and inside the cheeks. Taste buds in these locations are not always housed in papillae. Papillae containing taste buds have anywhere from a single taste bud to hundreds, and in total approximately 10,000 taste buds are distributed in the human mouth. The numbers of taste buds vary not only from person to person, but also vary with age. Infants have very few taste buds. The number peaks for adults in their forties, then begins to decline . Taste buds degenerate over time, lasting for about 10 days, and are constantly replaced, although they do not have axons projecting into the brain. Each taste bud averages 50 individual taste receptor cells, and sprouting from each taste receptor cell is a thread-like structure called the microvillus. A clump of microvillus extends into a tiny opening in the wall of the taste bud, which is bathed in saliva. It is the different types of saliva-borne chemical stimuli that produce different taste sensations (Blake & Sekuler, 2006).

Sensory transduction, the converting of chemical energy to electrical energy, varies with the stimulus type. Some ions are thought to enter the receptor membrane directly, altering the cell's electrical potential. Mucous secretions from supporting cells in the taste buds act as a cleansing agent and wash away excess stimulus substances from the vicinity of the taste bud. It is now known that different regions of the tongue are not associated with specific taste sensations. In actuality, there is a high degree of specificity between different receptors and different taste qualities. This specificity is seen when neural activity is recorded from the afferent nerves innervating taste receptors, and is also demonstrated by measuring chemical reactions in the receptors themselves. Finally, it appears some of the tongue receptors signal pain, touch, or temperature instead of taste. This is demonstrated by the burning sensation experienced when chewing a hot pepper. The receptor registers the presence of the active ingredient capsaicin, and signals from the receptor are then carried to the brain by fibers in a branch of the trigeminal nerve (Blake & Sekuler, 2006).

Taste is unique in that it sends neural messages over two cranial nerves. Fibers in one branch of the facial nerve, CN VII, innervate the front two-thirds of the tongue. Some of these fibers carry information from the left side of the tongue, and others from the right. The rear third of the tongue is innervated by fibers comprising the glossopharyngeal nerve, CN IX, also with different fibers innervating different sides of the tongue. Neural signals from non-tasting receptors are carried to the brain by the trigeminal nerve. The axons of the brainstem neurons innervated by these cranial nerves funnel taste-related information via two different pathways that mediate both aspects and consequences of taste perception. One pathway runs through a nucleus in the thalamus, and the second runs from the brain stem to the amygdala and the hypothalamus, structures that influence emotional responses to sensations and control appetite (Blake & Sekuler, 2006).

Taste responsive neurons in the thalamic nuclei that receive taste information are intermixed with other neurons that respond to tactile and or other thermal stimulations. All of these thalamic neurons project into the gustatory cortex, the primary taste area in the cerebral cortex. This area cannot be seen unless the temporal lobe is removed from both the parietal and frontal lobes by separating them along the lateral fissure. This will reveal the insula and the gustatory cortex. The exact location and boundaries of the primary taste area with the insula are difficult to locate, in part because taste stimuli also stimulate the touch system. The other cortical region for taste is located in the frontal cortex just above the eye orbits. Neurons in this secondary taste area signal taste attributes that are clearly behaviorally relevant. The orbito-frontal cortex is a general repository for information about behaviorally relevant dimensions of stimulation associated not only with taste but also with other sensory modalities (Blake & Sekuler, 2006).

Abnormalities and Implications of Gustatory Disorders

This section of the assignment will examine the implications of gustatory disorders on bulimia nervosa (BN) patients as well as its effects on immunity in the elderly.

The study on BN consisted of a cross-sectional study of 26 patents diagnosed with BN according to the DSM-IV and 26 healthy individuals in the control group, matching in age and body mass index. A statistically significant number of the BN subjects reported both disturbed salivary and taste profiles, including xerostomia (dry mouth), taste aberration, and burning sensation in the mouth. It is widely recognized that disturbances in the gustatory process are co-occurring in BN patients. Salivary composition alterations are known to significantly affect both taste perception and oral sensations. Despite these facts there has been minimal research on how taste perceptions and salivary abnormalities may either induce or exacerbate BN. The a priori hypothesis of the study was that changes in taste perception or salivary composition would be associated with a diagnosis of BN. Sixty-two percent of the control group did not complain of xerostomia, compared to 77% of the BN group. Further, 47% of the BN group complained of taste disturbances, compared to only 19% of the control group. Hence, an association was proven between the diagnosis of BN and the disturbance in gustation (Blazer, Latzer, & Nagler, 2008).

The loss of taste and smell that occur with advancing age can lead to poor appetite, inappropriate food choices, and decreased energy, all of which are associated with impaired protein and nutrient status and can lead to malnutrition. Taste and smell play a role in food choice and nutrient intake, prepare the body to digest food, enable us to detect foods with nutritional value, and enable the selection of a nutritious diet. Further, taste and smell initiate, sustain, and terminate ingestion, hence playing a role in the quantity of food eaten. Taste dysfunction in the elderly generally results from normal aging and from diseases such as cancer or from medications and environmental exposure. In most cases the sense of taste is reduced or impaired rather than totally absent. The incidence of the loss of taste and smell disorders will increase due to the projected growth in absolute and relative size of the older population (Schiffman & Graham, 2000).


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Blazer, T., Latzer, Y., & Nagler, R. M. (2008). Salivary and gustatory alterations among bulimia nervosa patients. European Journal of Clinical Nutrition, 62, 916-922. doi:10.1038/sj.ejcn.1602801

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