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Chapter 9: Chemical Senses: Olfaction and Gustation

Max O. Hutchins, Ph.D., Department of Integrative Biology and Pharmacology, McGovern Medical School

Reviewed and revised 07 Oct 2020

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An appreciation of the flavor of foods requires the diverse interaction of several sensory systems. Taste and smell are the principal systems for distinguishing flavors. However, tactile, thermal, and nociceptive sensory input from the oral mucosa contributes to food quality. Saliva also is an important factor in maintaining acuity of taste receptor cells (Figure 9.1). Its mechanisms of action include; acting as a solvent for polar solutes, transporting solutes to the taste receptors, buffering action for acidic foods and reparative action on the lingual epithelium.

Figure 9.1 Flavor of foods is dependent upon the oral sensory system, salivary secretion and mastication.

9.1 Gustatory System

Recent technical advances in neurophysiology have made it possible to identify the physiological mechanisms of signal transduction for the detection and discrimination of various taste stimuli by the taste receptor cells.

Figure 9.2 Generalized structure of a taste bud and cells.

Morphology of Taste Buds and Cell Types

Taste buds are located on papillae and distributed on the surface of the tongue. Taste buds are also found on the oral mucosa of the palate and epiglottis. These pear-shaped structures contain about 80 cells arranged around a central taste pore (Figure 9.2).

Taste receptor cells are spindle shaped, modified neuro-epithelial cells that extend from the base to the apex of the taste buds. Voltage-gated channel proteins for Na⁺, K⁺ & Ca²⁺ are present in the plasma membrane with the K⁺-gated channel proteins located in larger numbers on the apical membrane of the taste cells. Synaptic vesicles are present near the apex and the basal region in many taste cells. Microvilli from each taste cell project into the taste pore which communicate with the dissolved solutes on the surface of the tongue. These receptor cells are innervated by afferent nerve fibers penetrating the basal lamina. The nerve fibers branch extensively and receive synaptic input from the taste receptor cells. A group of non-receptor columnar cells and basal cells are present within taste buds. The basal cells migrate from adjacent lingual epithelium into the buds and differentiate into taste receptor cells which are replaced about every 9-10 days.

Transport of Solutes

Taste solutes are transported to the taste pore and diffuse through the fluid layer to make contact with membrane receptor proteins on the microvilli and apical membrane. Taste sensitivity is dependent upon the concentration of the taste molecules as well as their solubility in saliva. Many bitter tasting hydrophobic solutes interact with an odorant binding protein produced by von Ebner’s glands in the posterior region of the tongue.

Sensory Transduction

Taste sensation can be evoked by many diverse taste solutes. The pattern of membrane potential change include depolarization, depolarization followed by hyperpolarization, or only hyperpolarization. Action potentials in the taste receptor cells lead to an increase Ca²⁺ influx through voltage-gated membrane channels with the release of Ca²⁺ from intracellular stores. In response to this cation, neurotransmitter is released, which produces synaptic potentials in the dendrites of the sensory nerves and action potentials in afferent nerve fibers (Figure 9.3).

Salts

The taste of salts is mediated by Na⁺ ions which do not interact with a membrane receptor but diffuse through a Na⁺ channel located in the microvilli and apical membrane. Anions such as Cl^- contribute to the salty taste, but anions are transported into these cells by a paracellular route. The influx of these ions of salt evokes a depolarization in the apical membrane (Figure 9.3).

 

Figure 9.3 A taste receptor cell responding to Na+ salt.

Acids and Sour Tastes

The hydrogen proton of acids and sour foods can influx through the Na⁺ channels, or through a proton transport membrane protein (Figure 9.4). Some acids block the efflux of K⁺ at the microvilli. The resulting influx of protons or a reduction in K⁺ conductance will initiate receptor potentials in response to the quality of sour tastes.

Figure 9.4 A taste receptor cell responding to acid and sour solutes.

Sweet

Sweet tasting solutes, sugars and related substances, bind to membrane receptor proteins which are coupled to a G-s protein (gustducin), which activates adenylyl cyclase (AC). Cyclic AMP (cAMP) dependent protein kinase (PKA) reduces K⁺ efflux in the apical membrane and produces membrane depolarization (Figure 9.5). Some sweet solutes and non-sugar sweeteners interact with a receptor membrane protein through a G protein, which activates phospholipase C. A second messenger, inositol triphosphate (IP₃), is synthesized which releases Ca²⁺ from intracellular stores. Accumulation of Ca²⁺ depolarizes the cell, releasing neurotransmitter at the synapse.

Figure 9.5 A taste receptor cell responding to sweet solutes.

Bitter

Bitter tasting solutes include many non-toxic and toxic alkaloids, hydrophilic quinine and some divalent ions. The transduction of bitter tastes involves several mechanisms: 1) blockage of the efflux of K⁺ by a number of hydrophilic bitter substances generates a depolarizing potential; 2) interaction with a receptor membrane receptor coupled to the G protein, gustducin, and activation of cAMP dependent protein kinase with blockage of K⁺ channels; and 3) involves a receptor protein linked to G-protein and activation of phospholipase C, which results in substrate hydrolysis to IP₃, releasing Ca²⁺ from intracellular stores.

These mechanisms for taste transduction were identified in laboratory animals and are probably present in the microvilli and apical membrane of taste receptor cells in humans. A fifth taste quality, umami, is predicted to interact with a ligand-gated inotropic glutamate receptor coupled to gustducin and to Ca²⁺ channel membrane proteins.

Taste stimuli produce depolarizing and hyperpolarizing potentials in individual taste cells. Excitation of voltage-gated Na⁺, K⁺, and Ca²⁺ channels can generate action potentials which are propagated toward the basal region of the taste cell. These currents open the voltage-gated Ca²⁺ channels near the base of the taste cells, which leads to the subsequent release of neurotransmitter. These transmitters diffuse across the synaptic cleft and lead to the initiation of action potentials in the afferent nerve fibers.

Propagation of a Neural Code to the Gustatory Center

Historically, regional differences for each taste quality were predicted to exist on the tongue’s surface (e.g., sweet on the tip, sourness and salts on the sides, bitter in the posterior region). However, taste studies conducted on the neural response of whole cranial nerves demonstrate that a pattern of activity is produced by foods that are similar in taste. These patterns of activity are a clue to a taste code that occurs in many different taste cells and neurons responding to a particular taste stimulus. This finding indicates that no single fiber conducts only one taste quality (i.e., sweet, sour), although it may respond best to one quality and least to another. Recognition that branches of nerve fibers innervate several cells within and between taste buds indicates that a population of sensory nerve fibers activated by a taste stimulus transmits a neural code of the taste quality.

Branches of the facial cranial nerve, the chorda tympani, innervate taste buds in the anterior 2/3 of the tongue and part of the soft palate. The glossopharyngeal innervate the posterior 1/3 of the tongue. Both the vagus and glossopharyngeal nerves innervate the pharynx and epiglottis. Axons of these three cranial nerves terminate on 2^nd order sensory neurons in the nucleus of the solitary tract. From this site in the rostral medulla, axons project into the parabrachial nucleus in lower animals but not in humans. In humans, fibers of the 2^nd order neurons travel through the ipsilateral central tegmental tract to the 3^rd order sensory neurons in the ventroposterior medial nucleus (VPM) of the thalamus. The VPM projects to the ipsilateral gustatory cortex located near the post-central gyrus representing the tongue or to the insular cortex. See Figures 9.6 and 9.7.

Figure 9.6 Neural pathway for taste into the gustatory cortex.

Figure 9.7 Intensity of lights as an example of summed neural activity in each cranial nerve in response to a specific taste quality.

9.2 Olfactory System

The olfactory system in humans is an extremely discriminative and sensitive chemosensory system. Humans can distinguish between 1,000 to a predicted high of 4,000 odors. All of these odors can be classified into six major groups; floral, fruit, spicy, resin, burnt, and putrid (Refer back to Figure 9.1). The perception of odors begins with the inhalation and transport of volatile aromas to the olfactory mucosa that are located bilaterally in the dorsal posterior region of the nasal cavity.

Morphology of Olfactory Mucosa and Cell Types

The olfactory mucosa consists of a layer of columnar epithelium, surrounding millions of olfactory neurons, which are the only neurons to communicate with the external environment and undergo constant replacement. Basal cells near the lamina propria undergo differentiation and develop into these neurons about every 5-8 weeks. The glial-like columnar cells surround and support the bipolar neurons. These columnar cells have microvilli at their apex and secrete mucus which is layered on the surface of the olfactory mucosa (Figure 9.8).

Figure 9.8 The generalized structure of the olfactory mucosa and axons of olfactory neurons passing through the cribriform plate.

The bipolar olfactory neurons have a single dendrite which projects towards the apical mucosa. The terminal ending of the dendrites are flattened and have 5-25 cilia that are embedded in the mucosa on the surface. Each cilia may have as many as 40 specific receptor membrane proteins for interaction with different odorant molecules. The density of these receptors is enormous for humans, but significantly greater in many lower animals.

Dissolution of Odorant Molecules and Interaction with Sensory Receptors

Unbound hydrophilic odor molecules diffuse across the layer of mucus, whereas hydrophobic odors must become bound to a specific odorant binding protein to be transported to each cilium for interaction with specific receptors. All of these receptors have the same general structure, seven hydrophobic transmembrane regions, but the amino acid sequence within the cylinders spanning the membrane are extremely diverse which permits the discrimination of a large number of odors.

Transduction of Olfactory Stimuli

Odorant molecules bind reversibly to the diverse receptor membrane proteins which are coupled to a G-s group of proteins called G_olf. Activation of adenylyl cyclase leads to the formation of cAMP with the activation of Ca²⁺/ Na⁺ cation channels. The primary effect of influx of these ions is depolarization and the generation of a generator potential (Figure 9.9). Generated ionic currents are graded in response to the flow rate of the odorant molecules and to their concentration. Sites of summated generator potentials occur across the olfactory mucosa to produce specific spatial pattern of activity for each stimulating odorant molecules, which may contribute to neural coding of odors. These spatial responses across the olfactory mucosa can be recorded (electro-olfactograms) with surface electrodes.

Figure 9.9 Transduction of odorant molecules in an olfactory neuron to action potentials.

Propagation of Action Potentials and Convergence upon the Olfactory Bulb

The resulting influx of Na⁺ and Ca²⁺ produces a depolarizing generator potential that spreads to the axon hillock. There, action potentials are generated, which are propagated to the synaptic endings in the olfactory bulb (Figure 9.9).

Figure 9.10 Convergence of olfactory neuronal axons to synapse with mitral cells upon the glomeruli of the olfactory bulb.

The action potential frequency is proportional to the concentration of specific odorant molecules. However, action potential frequency will be attenuated by adaptation or desensitization of the receptor and reduction in the production of cAMP.

Rapid adaptation and removal of the odorants permit continued recognition and discrimination of new aromas that are inhaled in the next respiratory cycle. Action potentials generated in the axon terminals of activated neurons are propagated into the glomeruli within the olfactory bulb. The olfactory bulbs have many different types of neurons and these have a laminar distribution. On the ventral side of the olfactory bulbs is a layer of glomeruli. This is a site at which axon terminals of several thousand olfactory neurons synapse with numerous dendrites from large mitral cells and tufted cells. Interneurons such as the inhibitory periglomerular cells synapse with the nerve endings within adjacent glomeruli.

Millions of axon fibers converge upon only a few thousand glomeruli within each bulb to synapse with about 75,000 mitral cells (see Figure 9.10) and about twice this number of tufted/periglomerular cells. Mitral cells are 2^nd order sensory neurons whose axons enter the olfactory tract and ascend to the olfactory cortex. This convergence/divergence between the axons of olfactory neurons and the specialized cells of the olfactory bulb generate excitatory postsynaptic potentials (EPSPs) in the dendrites of mitral cells and subsequent action potentials. Lateral inhibition by the periglomerular cells modulates activity in adjacent glomeruli innervated by other mitral and tuft cells. A complex pattern of neuronal integration for discrimination of various odorant molecules is indicated by the mechanisms of convergence/divergence with excitation/inhibition of these 2^nd order sensory neurons. This complexity is related to the recognition that no single odor stimulates a specific group of olfactory neurons. Rather a neural code is created from the activation of multiple receptors and neurons.

9.3 Neural Pathway into the Olfactory Cortex

Figure 9.11 Projection of olfactory bulb into the olfactory cortex.

Axons from mitral and tuft cells project caudally into the olfactory tract. Fibers diverge and synapse with neurons of the anterior olfactory nucleus (AON). Axons from the AON cross to the opposite side of the hemisphere through the anterior commissure. The majority of the axons from the olfactory bulb diverge laterally and form the lateral olfactory tract which synapse with nuclei of the olfactory cortex. These are the piriform cortex (pc), the periamygdaloid cortex, part of the amygdala, and hippocampus. There are no direct relays from the olfactory bulb into the thalamus, but a few fibers synapse with 3rd order sensory neurons in the thalamic dorsomedial nucleus which are projected to the ipsilateral cerebral hemisphere (Figure 9.11).

9.4 Conclusion

In conclusion, many olfactory receptors respond to more than one odorant quality just like the taste receptor cells. Coding of the primary odor depends on the intensity of the odor and on a population response within the olfactory neurons. During neural processing in the olfactory bulb, a particular discharge occurs to one odorant and a different pattern for another odorant. This sensory input must be processed before being relayed to the olfactory cortex for perception and recognition of the individual odor.

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