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Gustatory System (continued)

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.