Taste and Smell Physiology

of 11 PHYSIOLOGY: TASTE & SMELL

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PART 1: SENSE OF SMELL I. HISTOLOGY/ ANATOMY

Figure 1. Olfactory sensory neurons embedded within the olfactory epithelium in the dorsal posterior recess of the nasal cavity. These neurons project axons to the olfactory bulb of the brain, a small ovoid structure that rests on the cribriform plate of the ethmoid bone.

Olfactory Mucous Membrane

Specialized portion of the nasal mucosa

Location of olfactory receptors

5-10 cm2 in the roof of nasal cavity near the septum (Ganong, 2000)

Contains: i. 10 – 20 million olfactory

receptors ii. Sustentacular cells

iii. Basal cells

Innervated by: i. Olfactory nerve – contains

olfactory receptor neurons ii. Trigeminal nerve – free nerve

endings which have nociceptor receptors

Olfactory receptor

Considered a neuron

Has short and thick dendrites with an olfactory knob (expanded portion at the tip of the dendrites)

Cilia arises from the olfactory rod

Axons pierce the cribriform plate of ethmoid bone and enter the olfactory bulbs. Bundles of axons comprise the olfactory nerve.

Life span is 30 – 60 days Cilia

Chemo-sensitive o Contains odorant receptors

Arises from the olfactory rod

Projects on the surface of the mucus

Unmyelinated processes (2μm long and 0.1 μm in diameter)

10 – 20 cilia/olfactory knob (Ganong, 1995)

Extensions of the plasma membrane of the olfactory vesicle

Figure 2. Structure of the olfactory epithelium. 3 cell types present: olfactory

sensory neurons, supporting cells, and basal stem cells at the base of the epithelium. Each sensory neuron has a dendrite that projects to the epithelial

surface. Numerous cilia protrude into the mucosal layer lining the nasal lumen.

A single axon projects from each neuron to the olfactory bulb. Odorants bind to specific odorant receptors on the cilia and initiate a cascade of events leading

to generation of action potentials in the sensory axon.

3 cell types in the olfactory mucosa:

1. Basal cells,

SUBJECT: PHYSIOLOGY

TOPIC: TASTE & SMELL PHYSIOLOGY

LECTURER: DR. DANTE SIMBULAN

DATE: MARCH 2011


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2. Sustentacular cells (helps to support the olfactory receptor neuron; serves as a structural and nutritional support for olfactory neurons), and

3. Basal cells 4. Bowman’s gland (minor cell which secretes

mucous) The axons of these neurons are TYPE C, so impulses conducted is very slow, relatively to other afferent neurons.

Olfactory Bulb

Location of olfactory glomeruli o Axons of olfactory receptors +

dendrites of mitral cells and tufted cells

Contains periglomerular cells o Inhibitory neurons connecting one

glumerolus to another

Contains granule cells o Doesn’t have axons o Makes reciprocal synapses with

lateral dendrites of mitral cells and tufted cells.

Cats and dogs have a strong sense of smell

Possibly the representation of olfactory receptor neuron in the brain of cats and dogs.

Larger surface area of the mucous membrane

Blessed to have a vomeronasal organ o Contributes to the regulation of the

reproductive cycle of other mammals—sensitive to pheromones on the air released by the opposite sex.

Contains 230,000,000 olfactory receptor neurons while in humans, there are only 10 to 20.

Characteristics of olfactory molecules:

Volatile o Transported by air

Water soluble o Penetrates the hydrated mucous

membrane of the nasal epithelium

Lipid soluble o Penetrates phospholipid bilayer of

olfactory receptor neurons to activate the cells.

Small (3-4 to 18-20 carbon atoms)

Different structural configurations give rise to different odors

So… the more water soluble and lipid soluble the odorants are, the more the stronger they smell.

Odorant Binding Proteins (OBP)

Seen within the mucous layer

Concentrate the odorants and transfer them to the receptors.

Accelerates the binding of olfactory molecules to the segment of the polypeptide chain of receptor proteins

There are also electrolytes present, which is responsible for the changes in the membrane conductance. All of the receptor potential involves movement of cations into the membrane during the depolarization process. Classification systems of olfactory stimuli

Odor Class Example of known compounds

Smells like

Floral Geraniol Roses

Ethereal Benzyl acetate Pears

Musky Muscone Musk

Camphor Cineole, camphor Eucalyptus

Putrid Hydrogen sulfide

Rotten eggs

Pungent Formic acid, acetic acid

Vinegar

This was an attempt by the scientists before to classify the different olfactory sensations, but sad to say, this was not enough. Current scientists have come up to about 100 to

1,000 primary sensation from which those 10,000 odorant molecules can be identified. They bind to olfactory receptor proteins in the cilia of the olfactory neurons. Current scientists say that this classification is not enough in classifying a more than

Just a clarification…

Cranial nerve I does not comprise the olfactory bulb and olfactory tract, it is the axons of the olfactory receptor neuron which comprise the olfactory bulb and tract. Olfactory neuron cells are not like taste cells, they are neurons. The taste cells are specialized epithelial cells. Both have short lifespan.

Fact: Pepperminty smell is due to stimulation of nerve fibers.


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10,000 odorant molecules which have already been recognized. II. RECEPTOR SENSITIVITY AND ADAPTATION

OF THE OLFACTORY RECEPTOR NEURON.

Sensitivity of the olfactory receptor neuron is not that

much sensitive in comparison to the somatosensory pathway. In the olfactory receptor neuron, once we identify it, it takes about 30% increase of concentration of the olfactory molecules before we notice the difference.

Substance mg/L of Air

Ethyl ether 5.83

Chloroform 3.30

Pyridine 0.03

Oil of peppermint 0.02

Iodoform 0.02

Butyric acid 0.009

Propyl mercaptan 0.006

Artificial musk 0.00004

Methyl mercaptan 0.0000004

Higher threshold = Less sensitive!

After reaching the threshold, even if we increase the concentration of 10, 20, 25, we will not be able to detect the change until we reach as much as 30% beyond the threshold.

STIMULUS TRANSDUCTION MECHANISM:

Recall that the cilia contain a metabotropic receptor which is embedded in the phospholipid membrane. These receptor proteins have the ability to bind a wide range of olfactory molecules.

Methyl mercaptan is mixed with propane gas which is a common household tool for cooking. It gives the LPG its characteristic odor when it leaks. Also, according to (Ganong, 1995), Methyl mercaptan also gives garlic its characteristic odor,

Adenylyl cyclase system

Depolarize


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Figure 3. Adenylyl Cyclase Pathway Most are metabotropic receptors acting as molecular sites for binding of different molecules. In this case, cAMP will help in phosphorylation reactions which will change the structure of protein subunits of cation channels, allowing the influx to cause depolarization and then generation of receptor potential.

Figure 4. IP3 Pathway Not only the adenylyl cyclase is involved, phospholipase C is also involved in activating the olfactory neuron. If IP3 is involved, inositol triphosphate acts to some receptors of the ER to open the calcium stores to release calcium, which helps in depolarizing the cell.

In this case, there is no myelin sheath in the olfactory receptor neuron because it is a type C, so sa axon hilux or sa initial segment lang siya nag-gegenerate dahil wala naming nodes of ranvier. III. DISCRIMINATION OF ODOR INTENSITY

AND QUALITY; ODOR STIMULUS LOCALIZATION

How can the olfactory system discriminate more than 10,000 kinds of odorant molecules? Olfactory neurons utilize a large number of G-protein-

coupled receptor molecules to detect a wide range of odors. About 1,000 genes encode and produce 1,000 Olfactory receptor proteins. (About 1 % of Human genome). There are about 1,000 olfactory receptor cell

types, each one producing a protein. Each olfactory receptor proteins bind to an array of these odorant molecules, which explains why we can distinguish about 10,000 or more different odors.

The olfactory system recognizes and interprets patterns

of responses by neurons in the ascending pathways. Different odor qualities and concentrations can be detected by patterns of responses and not just by a simple labeled-line mechanism (which is the case for the somatosensory system).

Figure 5. These patterns of responses by 2nd order neurons of the olfactory pathway are partly “shaped” by the inhibitory interneurons of the olfactory bulb (periglomerular and granule cells). This is an example of lateral inhibition in the olfactory system.

1st order neurons = Olfactory receptor neuron 2nd order neurons = Mitral Cell

Odor A – When our olfactory receptor is exposed to an odor stimulus with a high concentration of 1 molecule, the spike discharge has a higher response in the 1st order neuron compared to the 2nd order neuron. In the 2nd order neuron manifests a rapidly adapting response – so we can see that there is a desensitization mechanism because of the very strong smell. Our CNS has the ability to stop the barrage of signals so that we won’t be overwhelmed with the smell. Odor B – There is a basal activity in the 1st order neuron but stops as the impulse reaches the 2nd order neuron. Somehow there is still a manifestation of odor signal, so there can either be a discharge recognized by CNS or an association of discharge because there is a basal activity in the 1st order neuron. Odor C: No response for both. So these are just tonic or resting discharges.

Why can we LOCALIZE source of odor stimuli ?

So this experiment concludes that the Olfactory receptor neurons respond in different ways depending on the molecule. With 3 molecules, they respond differently.

Please refer to Dr. Simbulan’s handout on Taste & Smell for the diagram and for a more in depth discussion regarding adaptation.


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Crude Topographic Representation of Olfactory Receptor Cells in the olfactory bulb give spatial information about stimuli. IV. ADAPTATION MECHANISMS:

It is rapidly adapting, but in Guyton & Hall, it is partially adapting.

Adaptation mechanisms can take place in 2 levels:

1. Receptor level 2. CNS at the olfactory bulb level

Adaptation mechanisms at the peripheral level:

(1) Phosphorylation of kinases prevents the

interaction of G-protein and portion of polypeptide chain of receptor

Kinase causes the phosphorylation of polypeptide chain and therefore will change in conformation. This prevents the access to the binding site of G-protein. The cascade stops even if the odorant molecule binds to the receptor.

(2) Desensitization of cAMP

Constant depolarization due to an increased intracellular calcium, causes the activation of calcium-calmodulin complex that will allow its binding to cAMP sensitive cation channels. This will desensitize the cation channel’s response to cAMP, so the cation channels remain open.

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Adaptation mechanisms arising from inhibitory signals from CNS structures:

1. Periglumerolar cells and granule cells are

inhibitory neurons and are activated by some descending inputs from the olfactory cortex. So when there is a barrage of strong smells, ascending inputs can be inhibited by both ascending and lateral inhibition mechanism. It

can prevent inflow of signals from 1st order neurons to 2nd order neurons.

Summary:

The axons of the olfactory receptor neuron terminate in the olfactory bulb, specifically in the olfactory glomeruli

(which form synapses with mitral and tufted cells in the olfactory bulb) The 2nd order neurons (mitral & tufted cells) of the olfactory bulb projects to the olfactory cortex. (Again, read more on lateral inhibition and descending

inhibition by periglomerular and granule cells in the olfactory bulb, ―shaping‖ the responses of 2nd-order neurons.)

Axons of mitral and tufted cells comprise the olfactory tract. In animals, the vomeronasal organ is connected to another pathway. The human olfactory cortex helps in sensory discrimination of olfactory system. From the olfactory cortex, olfactory information reaches other cortical areas via the thalamus (and hypothalamus). [Unique to olfaction, note that the thalamus does not serve as a relay from receptor to olfactory cortex.]

Olfactory information, from bilateral sides of olfactory cortex, is also conveyed via the thalamus with greater projection to and activation of the right side of the

orbitofrontal cortex . This is for conscious olfactory perception and discrimination. 5 main areas of the olfactory cortex and functions: 1. Anterior olfactory nucleus


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An integrative center connecting the two olfactory bulbs through the anterior commissure; integration of olfactory inputs; information-sharing

2. Piriform cortex

Main area involved in olfactory discrimination; electrical stimulation in humans produces olfactory sensations.

3. Olfactory tubercle

Involved in various functions of limbic system; also receives ascending dopaminergic inputs from the midbrains; malfunction in this area leads to kinds of schizophrenia.

4. Amygdala

Its corticomedial parts receive inputs from the main and accessory olfactory bulbs; emotional responses to olfactory stimuli.

5. Part of enthorhinal cortex

Receives olfactory input and projects to hippocampus;

Involved in olfactory memories. V. DISORDERS OF THE SENSE OF SMELL

1. Anosmia – loss of sense of smell by injury or disease. 2. Hyposmia - a reduced sense of smell, frequently associated with heavy smoking. Anosmias and hyposmias can be due to:

a. Conductive Deficit i. Processes that prevent odorants

from reaching the olfactory epithelium

ii. Example: 1. Nasal Polyps 2. Septal deviations 3. Inflammations during

the common cold b. Sensorineural Deficit

i. Processes that damage olfactory receptor neurons or parts of the olfactory CNS

ii. Example: 1. Head injuries

2. Neurological disorders such as Parkinson’s and Alzheimer’s

Any lesions cause anosmia. Age-related changes in smell also occur as a result of decreased number of cells in olfactory bulb and nasal lining.

Please refer to the diagram on your right so you guys can fully visualize the areas of the olfactory cortex.


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PART 2: SENSE OF TASTE

I. HISTOLOGY/ANATOMY

Taste buds

Composed of 50 modified epithelial cells:

Sustentacular

Taste cells

The outer tips of taste cells are arranged a round a small taste pore, which has microvilli at the tip that protrudes outward from the taste pore.

At the body of the taste cells, there is a branching terminal network of taste nerve fibers that are stimulated by the taste receptor cells.

It is found on the 3 types of papillae of the tongue

Circumvalate papilla

Fungiform papilla

Foliate papilla

It can also be found in the palate, tonsillar pillars, epiglottis, proximal esophagus.

Beyond the age of 45, many taste bids degenerate

There are 40 to 60 cells per taste bud.

They have a short lifespan (10 days to 14 days), but are replenished by basal cells.

Figure 1. Anatomical features of the taste bud. Each taste bud is made up of 4 types of cells: Basal cells; Type 1 & Type 2 cells (sustentacular cells); Type 3 cells (gustatory receptor cells that make up synaptic connections to sensory nerve fibers); Von Ebner’s gland (secretes mucous mixture that contains proteins).

Various taste buds are located in the oral cavity and walls of pharynx. The oral cavity is innervated by various cranial nerves. Taste buds cell are situated on the posterior, anterior, lateral portions of the tongue.

Location of taste bud Innervation

Pharyngeal wall Vagus nerve

Epiglottis Vagus nerve

Palate Facial nerve

Tongue

a. Anterolateral portion b. Posterior portion

Glossopharyngeal Facial nerve

Figure 2. Distribution of taste buds in human oral cavity and its corresponding afferent nerves

Tongue Map

Areas of the tongue respond to various taste stimuli. For decades, there was a traditional tongue map which was shown both in medical, elementary, high school, and college. In the map, there is a regional distribution of sensitivities. Sensitivity shown here is no longer valid. However the innervation of the tongue is still correct.

II. QUALITY AND CLASSES OF GUSTATORY STIMULI

Classes of taste stimuli: 1. Sour tasting substances

Mainly sensitive to hydrogen containing substances such as Acids (H+).

Intensity of the taste is proportional to the concentration of hydrogen ions. The more acidic the food, the more sour it gets.

2. Salty tasting substances

Sodium-containing substances (Na+), as well as some organic compounds (e.g. lysyltaurine, ornithyltaurine)

Cations of the salts (Na cations) are mainly responsible for the salty taste, but anions also do contribute but in a lesser extent.


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3. Sweet tasting substances

Mostly organic (sucrose, maltose, lactose, glucose , other polysaccharides; some proteins; also lead salts, artificial sweeteners)

Slight changes in chemical structure can often change the substance from sweet to bitter.

4. Bitter tasting substances

Organic substances such as morphine, Nicotine, caffeine, urea; inorganic salts of magnesium. Ammonium, and calcium (due to cation).

There are 2 particular class of substances are especially likely to cause bitter taste:

- Long-chain organic substances that contain nitrogen

- Alkaloids (include many of the drugs used in medicines such as quinine, caffeine, strychnine, nicotine)

5. Umami tasting substances

Taste sensation produced by glutamate and glutamate-like substances, found in seaweeds and other seafoods.

Facial nerve is more sensitive to: Sugar > Salty and sour > bitter

Glossopharyngeal nerve is more sensitive to: Sour and bitter > sweet and salty Vagus nerve is more on pharynx

In regurgitation, we can actually taste it – so it is a somatosensory feeling. It's a real taste sensation when we feel the acid from our stomach to our pharynx.

Sensation is also sensitive to water – it is also mapped out as one of the taste stimuli

III. Taste Thresholds and Intensity Discrimination

Substance Taste Threshold Concentration (μmol/L)

Hydrochloric acid Sour 100

Sodium Chloride Salt 2,000

Strychnine hydrochloride

Bitter 1.6

Glucose Sweet 80,000

Sucrose Sweet 10,000

Saccharin Sweet 23

Figure 3. We have a low threshold for Saccharin (an artificial sweetener), which makes us more sensitive. High threshold means lower sensitivity to substances and low threshold means higher sensitivity.

So basically, substances that are edible and have nutritive value have a relatively higher threshold to substances that are toxic. This is important so that we won’t be overwhelmed with the taste of the food, to the extent that we might reject or stay away from it. Also, toxic substances such as HCl have a low threshold (therefore high sensitivity) so that we are able to detect it, and therefore it prevents from burning our GIT. Saccharin is an artificial molecule and has been withdrawn from the market. Saccharin was in many products which are calorie free. Aspartate has replaced saccharine. It came back. Sometime it was banned from the market because it was carcinogenic. We also have low threshold for bitter substances.

Glycine chloride binding receptor antagonist - blocks inhibitory neurotransmitter glycine so we may have convulsion

toxic, use for malaria

Nicotine - toxic doses if increased sensations. Some bitter substances can have antioxidant properties, but some are toxic. So, bitter taste has higher sensitivity and low threshold. IV. General transduction Mechanisms by Gustatory

Receptor Cells

(1) Interaction of taste stimuli with the apical membrane either by:

Binding to G-protein coupled receptors Modulating apically located ion channels There are 13 types of chemical receptor

proteins in taste bud cells:

2 sodium receptors

2 potassium receptors

1 chloride receptor

1 adenosine receptor

1 inosine receptor

2 sweet receptors

2 butter receptors

1 glutamate receptor

1 hydrogen ion receptor

Primary sensation of taste is used for practical analysis of taste, so it can also be grouped into 5 general categories

Sour

Salty


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Sweet

Bitter

Umami

Molecular characteristics of receptors:

Taste Sensation

Ionotropic Receptor

Metabotropic Receptor (G-protein coupled)

Salty Yes

Sour Yes

Sweet Yes

Bitter Yes

Umami Yes

(2) Generation of Receptor Potential:

Change in electrical potential in the taste cell.

Membrane of taste cell is negatively charged on the inside with respect to the outside. Application of taste substance to the taste hairs causes depolarization.

In most cases, the decrease in potential (therefore decrease in depolarization) is proportional to the concentration of the stimulating substance.

Mechanism:

Binding of taste chemical to protein receptor molecule of taste receptor cell

Causes the entrance of Na+ ions or H+ ions causes depolarization

MECHANISM FOR SALTY SUBSTANCES: 2 types of taste receptor proteins are located in the apical portion of taste receptor cells: ionotropic & metabotropic channel receptors. Na+ enters the Amiloride-sensitve ENaC (Epithelial Na+ Channels). When Na+ binds to ionotropic taste receptors, it causes immediate depolarization, while binding Na+ to metabotropic receptors requires the activation of 2nd messengers for the taste receptor cells to be depolarized which will then release neurotransmitter for activation of 1st order neuron. Glutamate is usually released (excitatory to nerve endings for glossopharyngeal, facial, and vagus nerve) *Amiloride is a potassium-sparing diuretic which manages hypertension and congestive heart failure. It works by directly blocking ENaC, thereby inhibiting Na+ reabsorption in the late distal convoluted tubules, connecting tubules, collecting ducts in the kidney.

MECHANISM FOR SOUR TASTE: There are no H+ ion channels to which they pass. In this case, they block potassium channels, which causes depolarization. 2 ways of depolarizing the membrane:

1. Potassium channel is blocked by H+ a. There is a build up of positive ions,

especially if Na-K pump is active, which brings potassium more inside and sodium outside.

2. Entrance of H+ in through ENaC

a. CNS is the one responsible for giving the taste sensation, not the ENaC. So, ENaC which is originally seen in the pathway for salty substance does not cause the salty taste in this area. For every taste sensation, there is a specific cortex which is responsible for a specific taste.


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MECHANISM FOR SWEET TASTE:

1. Adenylyl cyclase/ cAMP pathway: Glucose binds to membrane receptros, coupled with G-proteines, activate adenylyl cyclase and reasie cAMP intracellularly. cAMP activates protein kinase A, which phosphorylates K+ channels, reducing K+ conductance. This results to membrane depolarization (causing receptor potential)

2. Phospholipase C/IP3, DAG pathway:

Artificial sweeteners activate phospholipase C, which produce 2nd messenger !P3 and diacylglycerol (DAG). Ip3 causes release of Ca 2+ from intracellular stores, while DAG activates protein kinase C. The release of intracellular Ca 2+ stores from endoplasmi reticulum results in release of transmitter substance.

3. Some sugars may also directly gate cation channels without 2nd messengers.

MECHANISM FOR BITTER TASTE

There may be as many as 24 G-protein-linked bitter receptors in humans. Some examples below.

1. PLC/ IP3-DAG Pathway: Denatonium (bitter-tasting molecule), interacts with a G-protein-coupled receptor, which activates phospholipase

C (PLC), producing IP3 (2nd messenger). IP3 increases intracellular Ca 2+ levels, leading to release of synaptic transmitter, and activation of gustatory nerve fiber.

2. Phosphodiesterase activation Denatonium binds to a G-protein (gustducin) - coupled receptor, activating phosphodiesterase, causing a decrease in cAMP; cAMP block of cation channels is

removed, resulting in cation influx.); PDE = phosphodiesterase; PDE reduces cAMP concentration. (receptor = T2R class)

MECHANISM FOR UMAMI TASTE

Metabotropic receptors and ionotropic receptors of glutamate.

There are 2 mechanisms for this taste: 1. One mechanism: (Boron) Glutamate binds to a glutamate-gated (ionotropic receptor type), nonselective cation channel, opening it and producing depolarization. This further activates transmembrane voltage-gated calcium ion channels, raising the intracellular calcium ion concentration, leading to transmitter release from the taste cell. This in turn activates the afferent nerve endings. 2. Another mechanism: Activation of a truncated metabotropic

glutamate receptor (mGluR4) in the taste buds, with agonists being purine 5-ribonucleotides such as IMP and GMP in the food. Mechanism of depolarization through this mechanism unsettled.

V. DISCRIMINATION OF TASTE QUALITY &

INTENSITY

Each nerve fiber in the gustatory nerves responds to more than one taste stimuli.


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However, each fiber responds best to one of the four primary taste qualities.

The coding of a gustatory sensation (taste quality) is not a simple, labeled-lined mechanism. It is a pattern of activities in nerve fibers activated by a particular stimulus.

Taste stimulus intensity discrimination is crude, as it takes a 30% increase in concentration before a difference in taste stimuli intensity is detected. Note similarity with smell discrimination.

a. Example: Increasing the salt concentration by another 5%, 10% and 20%, it will remain undetected unless we increase it by 30%

VI. TASTE RECEPTOR CELLS EXHIBIT A RAPID

ADAPTATION MECHANISM

Adaptation of the gustatory system (almost complete, within a minute or so of continuous stimulation) results from: a. Sensory adaptation (ADAPTATION at the level of the taste bud cells) b. Central adaptation (adaptation at the level of higher-order neurons in the CNS) Why don't we normally lose sense of taste for good food?

Before the end of taste stimuli, there is a gradual decline or changes in response to taste receptors cells. There's always a constant stimuli in our taste bud cells, representing various taste. Taste receptor cells are rapidly adapting. VII. SUMMARY OF ASCENDING TASTE

PATHWAY

1. The first-order neurons: The taste fibers of Nerves VII and IX terminate in, or in the vicinity of the nucleus tractus solitarius (NTS) of the medulla oblongata. 2. The second-order neurons: The NTS is connected, by way of the ipsilateral medial lemniscus, with the Thalamus (in the region of the ventral posteromedial nucleus, VPM, of thalamus).

3. The third-order neurons

Pass through the internal capsule and terminate in the region of the ipsilateral postcentral gyrus in the face area of the Parietal Cortex . The 3rd order neurons also project to the anterior part of the insular cortex; this area is said to mediate conscious perception of taste and taste

discrimination ).

Reflexes are mediated by nucleus tractus solitarius anterior insula Lesions in the anterior insula (foot of postcentral gyrus) - we lose taste sensation VIII. DISORDERS OF THE SENSE OF TASTE:

1. Ageusia – absence of sense of taste. 2. Hypogeusia – diminished taste sensitivity

Short lifespan - taste bud cells are replenished by basal cells. If basal cells are diminished, there is reduced in the ability to generate sensor cells thus we lose taste sensitivity as we get older. Lifestyle is also a factor. Synthetic sense of flavor:

The culinary experience is an integration of sensory inputs: Smell, sight, tactile, thermal, and memory, and even the emotional aspect.

END OF TRANSCRIPTION

If the diagrams are not clear, please refer to Dr. Simbulan’s handout regarding Taste & Smell physiology and also to the book of Ganong.

Goodluck 2014! I hope this helped you a lot! Hoping STD has inspired you to study harder and help those who are in need so we can have a

100% passing in the boards! Happy Studying!

Taste and Smell Physiology

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