What Specific Receptor Cells Respond to Chemicals Dissolved in Saliva?

Affiliate 9: Chemical Senses: Olfaction and Gustation

Max O. Hutchins, Ph.D., Section of Integrative Biological science and Pharmacology, The UT Medical School at Houston

Reviewed and revised 07 Oct 2020

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An appreciation of the flavor of foods requires the various interaction of several sensory systems. Taste and scent are the main systems for distinguishing flavors. Withal, tactile, thermal, and nociceptive sensory input from the oral mucosa contributes to food quality. Saliva also is an important factor in maintaining vigil of taste receptor cells (Figure 9.ane). Its mechanisms of action include; acting as a solvent for polar solutes, transporting solutes to the sense of taste receptors, buffering activeness for acidic foods and reparative action on the lingual epithelium.

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

9.1 Gustatory System

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

Effigy 9.2 Generalized structure of a taste bud and cells.

Morphology of Taste Buds and Cell Types

Gustatory modality buds are located on papillae and distributed on the surface of the natural language. Sense of taste buds are also found on the oral mucosa of the palate and epiglottis. These pear-shaped structures incorporate almost 80 cells bundled effectually a primal 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⁺, Chiliad⁺ & Ca²⁺ are present in the plasma membrane with the K⁺-gated aqueduct proteins located in larger numbers on the apical membrane of the gustatory modality cells. Synaptic vesicles are present almost the apex and the basal region in many taste cells. Microvilli from each sense of taste prison cell project into the taste pore which communicate with the dissolved solutes on the surface of the tongue. These receptor cells are innervated past afferent nerve fibers penetrating the basal lamina. The nervus fibers branch extensively and receive synaptic input from the gustatory modality receptor cells. A group of non-receptor columnar cells and basal cells are present within taste buds. The basal cells migrate from next lingual epithelium into the buds and differentiate into gustation receptor cells which are replaced about every 9-10 days.

Transport of Solutes

Taste solutes are transported to the gustation 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 sense of taste molecules besides as their solubility in saliva. Many biting tasting hydrophobic solutes interact with an odorant binding protein produced past von Ebner's glands in the posterior region of the tongue.

Sensory Transduction

Sense of taste sensation tin can be evoked by many diverse gustatory modality 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 increment 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 activeness potentials in afferent nervus fibers (Figure 9.3).

Salts

The gustatory modality of salts is mediated by Na⁺ ions which do non collaborate 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 sense of taste, only anions are transported into these cells by a paracellular route. The influx of these ions of salt evokes a depolarization in the apical membrane (Effigy 9.3).

Figure nine.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 (Effigy 9.4). Some acids block the efflux of Thou⁺ 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 gustation receptor cell responding to acrid and sour solutes.

Sweetness

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 1000⁺ efflux in the apical membrane and produces membrane depolarization (Effigy ix.5). Some sweetness solutes and non-sugar sweeteners interact with a receptor membrane poly peptide through a G protein, which activates phospholipase C. A 2nd 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 sweetness solutes.

Biting

Biting tasting solutes include many not-toxic and toxic alkaloids, hydrophilic quinine and some divalent ions. The transduction of biting tastes involves several mechanisms: 1) blockage of the efflux of K⁺ by a number of hydrophilic biting substances generates a depolarizing potential; 2) interaction with a receptor membrane receptor coupled to the Yard 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 Caⁱⁱ⁺ from intracellular stores.

These mechanisms for taste transduction were identified in laboratory animals and are probably nowadays in the microvilli and upmost membrane of taste receptor cells in humans. A 5th taste quality, umami, is predicted to interact with a ligand-gated inotropic glutamate receptor coupled to gustducin and to Ca²⁺ aqueduct membrane proteins.

Gustation stimuli produce depolarizing and hyperpolarizing potentials in private gustation cells. Excitation of voltage-gated Na⁺, K⁺, and Ca^two+ channels can generate activity potentials which are propagated toward the basal region of the taste prison cell. These currents open the voltage-gated Caⁱⁱ⁺ 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 activity potentials in the afferent nerve fibers.

Propagation of a Neural Lawmaking to the Gustatory Centre

Historically, regional differences for each gustation quality were predicted to exist on the tongue'southward surface (e.g., sweet on the tip, sourness and salts on the sides, biting in the posterior region). However, taste studies conducted on the neural response of whole cranial nerves demonstrate that a pattern of activity is produced past foods that are like in taste. These patterns of action are a clue to a taste lawmaking that occurs in many dissimilar taste cells and neurons responding to a item taste stimulus. This finding indicates that no single fiber conducts but one taste quality (i.e., sweet, sour), although it may answer best to one quality and to the lowest degree to another. Recognition that branches of nerve fibers innervate several cells within and betwixt taste buds indicates that a population of sensory nerve fibers activated by a sense of taste stimulus transmits a neural code of the taste quality.

Branches of the facial cranial nerve, the chorda tympani, innervate sense of taste buds in the inductive 2/iii of the tongue and part of the soft palate. The glossopharyngeal innervate the posterior ane/3 of the natural language. Both the vagus and glossopharyngeal fretfulness innervate the pharynx and epiglottis. Axons of these three cranial nerves finish on 2^nd lodge 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-fundamental gyrus representing the tongue or to the insular cortex. See Figures 9.6 and ix.seven.

Figure 9.6 Neural pathway for taste into the gustatory cortex.

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

ix.2 Olfactory Organisation

The olfactory organization in humans is an extremely discriminative and sensitive chemosensory organization. Humans can distinguish between one,000 to a predicted high of 4,000 odors. All of these odors tin be classified into 6 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 Jail 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 almost the lamina propria undergo differentiation and develop into these neurons virtually every v-viii weeks. The glial-like columnar cells surround and back up 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).

Effigy 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 unmarried 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, merely significantly greater in many lower animals.

Dissolution of Odorant Molecules and Interaction with Sensory Receptors

Unbound hydrophilic odor molecules lengthened across the layer of fungus, 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 construction, vii hydrophobic transmembrane regions, merely the amino acid sequence inside 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 various receptor membrane proteins which are coupled to a M-s group of proteins chosen G_olf. Activation of adenylyl cyclase leads to the formation of army 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 blueprint of activeness for each stimulating odorant molecules, which may contribute to neural coding of odors. These spatial responses beyond the olfactory mucosa tin exist recorded (electro-olfactograms) with surface electrodes.

Effigy 9.9 Transduction of odorant molecules in an olfactory neuron to activeness potentials.

Propagation of Action Potentials and Convergence upon the Olfactory Seedling

The resulting influx of Na⁺ and Ca²⁺ produces a depolarizing generator potential that spreads to the axon hillock. In that location, action potentials are generated, which are propagated to the synaptic endings in the olfactory bulb (Figure nine.9).

Figure ix.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, activity 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 connected recognition and bigotry of new aromas that are inhaled in the adjacent respiratory cycle. Activity potentials generated in the axon terminals of activated neurons are propagated into the glomeruli inside 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 big mitral cells and tufted cells. Interneurons such as the inhibitory periglomerular cells synapse with the nervus endings within adjacent glomeruli.

Millions of axon fibers converge upon just a few thousand glomeruli within each seedling to synapse with virtually 75,000 mitral cells (see Figure 9.x) and nigh 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/difference 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 activity potentials. Lateral inhibition by the periglomerular cells modulates activeness in adjacent glomeruli innervated past other mitral and tuft cells. A circuitous design 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 complication is related to the recognition that no single odor stimulates a specific grouping of olfactory neurons. Rather a neural code is created from the activation of multiple receptors and neurons.

nine.iii Neural Pathway into the Olfactory Cortex

Figure nine.11 Projection of olfactory seedling 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 grade the lateral olfactory tract which synapse with nuclei of the olfactory cortex. These are the piriform cortex (pc), the periamygdaloid cortex, function 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 (Effigy 9.eleven).

9.4 Decision

In conclusion, many olfactory receptors respond to more than i odorant quality just like the gustatory modality receptor cells. Coding of the primary olfactory property depends on the intensity of the olfactory property and on a population response within the olfactory neurons. During neural processing in the olfactory bulb, a particular discharge occurs to 1 odorant and a different pattern for another odorant. This sensory input must be candy earlier being relayed to the olfactory cortex for perception and recognition of the private aroma.

Test Your Knowledge

• Question 1
• A
• B
• C
• D
• Eastward

Second-social club sensory neurons for taste are located in the

A. Insula

B. Amygdala

C. Nucleus solitarius

D. Uncus

Eastward. Trigeminal ganglion

2d-society sensory neurons for gustatory modality are located in the

A. Insula This answer is INCORRECT.

The insula is not the site for the 2nd order neurons but does take gustatory and autonomic areas.

B. Amygdala

C. Nucleus solitarius

D. Uncus

E. Trigeminal ganglion

2d-club sensory neurons for taste are located in the

A. Insula

B. Amygdala This answer is Wrong.

The amygdala is a main component of the limbic system and has areas for olfaction.

C. Nucleus solitarius

D. Uncus

E. Trigeminal ganglion

Second-order sensory neurons for taste are located in the

A. Insula

B. Amygdala

C. Nucleus solitarius This answer is Right!

Afferents from the 1st order sensory neurons of the facial, glossopharyngeal and vagus nerves cease on the 2nd order neurons int he nucleus solitarius.

D. Uncus

East. Trigeminal ganglion

Second-order sensory neurons for gustation are located in the

A. Insula

B. Amygdala

C. Nucleus solitarius

D. Uncus This answer is Wrong.

The uncus is a small gyrus near the olfactory cortex.

E. Trigeminal ganglion

2nd-order sensory neurons for sense of taste are located in the

A. Insula

B. Amygdala

C. Nucleus solitarius

D. Uncus

E. Trigeminal ganglion This reply is INCORRECT.

Get-go-order sensory neurons for sensory input from the orofacial region are located in this large ganglion.

• Question ii
• A
• B
• C
• D

All of the following statements are correct about the olfactory receptor neurons EXCEPT:

A. These specialized neurons are replaced nearly every 5- eight weeks.

B. Each neuron contains receptors which are specific for a single odorant molecule.

C. The axon of each olfactory neuron synapses in only one glomerulus in the olfactory bulb.

D. Odorant molecules interact with receptors coupled to a K protein chosen Golf.

All of the following statements are correct nearly the olfactory receptor neurons EXCEPT:

A. These specialized neurons are replaced almost every 5- 8 weeks. This is Not the exception.

Olfactory neurons are replaced by basal cells.

B. Each neuron contains receptors which are specific for a unmarried odorant molecule.

C. The axon of each olfactory neuron synapses in only one glomerulus in the olfactory seedling.

D. Odorant molecules interact with receptors coupled to a 1000 protein chosen Golf game.

All of the following statements are right near the olfactory receptor neurons EXCEPT:

A. These specialized neurons are replaced about every 5- viii weeks.

B. Each neuron contains receptors which are specific for a single odorant molecule. This IS the exception, and is an incorrect statement!

Olfactory receptors interact with many dissimilar odorant molecules with the generation of a neural code that permits usa to discriminate between odors.

C. The axon of each olfactory neuron synapses in only one glomerulus in the olfactory seedling.

D. Odorant molecules collaborate with receptors coupled to a Thousand protein called Golf game.

All of the post-obit statements are correct almost the olfactory receptor neurons EXCEPT:

A. These specialized neurons are replaced about every v- 8 weeks.

B. Each neuron contains receptors which are specific for a single odorant molecule.

C. The axon of each olfactory neuron synapses in only one glomerulus in the olfactory bulb. This is Non the exception.

Axons of each olfactory neurons interact with simply one glomerulus.

D. Odorant molecules interact with receptors coupled to a G protein chosen Golf.

All of the following statements are correct about the olfactory receptor neurons EXCEPT:

A. These specialized neurons are replaced about every 5- 8 weeks.

B. Each neuron contains receptors which are specific for a single odorant molecule.

C. The axon of each olfactory neuron synapses in only one glomerulus in the olfactory seedling.

D. Odorant molecules interact with receptors coupled to a Yard protein chosen Golf game. This is Non the exception.

Receptors interact with and produce a release of active Thou-protein which activate military camp.

• Question 3
• A
• B
• C
• D

Which of the following cells are 2d gild neurons with axons projecting into the anterior olfactory cortex?

A. Mitral cells

B. Glomerular cells

C. Periglomerular cells

D. Granule cells

Which of the following cells are second lodge neurons with axons projecting into the anterior olfactory cortex?

A. Mitral cells This reply is CORRECT!

Mitral cells and tufted cells in the lamina of the olfactory bulb ship axons into the olfactory cortex.

B. Glomerular cells

C. Periglomerular cells

D. Granule cells

Which of the following cells are second order neurons with axons projecting into the inductive olfactory cortex?

A. Mitral cells

B. Glomerular cells This respond is CORRECT!

There are no glomerular cells in the olfactory bulb, but a site where many olfactory receptor neurons converge on the mitral and tufted cells.

C. Periglomerular cells

D. Granule cells

Which of the post-obit cells are 2nd order neurons with axons projecting into the anterior olfactory cortex?

A. Mitral cells

B. Glomerular cells

C. Periglomerular cells This answer is Wrong.

The periglomerular cells are inhibitory and by lateral inhibition command output from the glomeruli.

D. Granule cells

Which of the following cells are 2nd order neurons with axons projecting into the anterior olfactory cortex?

A. Mitral cells

B. Glomerular cells

C. Periglomerular cells

D. Granule cells This answer is Incorrect.

The granule cells also modulate activity from the mitral cells and tufted cells.

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Source: https://nba.uth.tmc.edu/neuroscience/m/s2/chapter09.html

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