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SUBJECT: PHYSIOLOGY

TOPIC: TASTE & SMELL PHYSIOLOGY


LECTURER: DR. DANTE SIMBULAN
DATE: MARCH 2011

PART 1: SENSE OF SMELL  Cilia arises from the olfactory rod


 Axons pierce the cribriform plate of
I. HISTOLOGY/ ANATOMY 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 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 Figure 2. Structure of the olfactory epithelium. 3 cell types present: olfactory
ii. Trigeminal nerve – free nerve sensory neurons, supporting cells, and basal stem cells at the base of the
endings which have nociceptor epithelium. Each sensory neuron has a dendrite that projects to the epithelial
surface. Numerous cilia protrude into the mucosal layer lining the nasal lumen.
receptors 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
Olfactory receptor to generation of action potentials in the sensory axon.
 Considered a neuron
 Has short and thick dendrites with an
olfactory knob (expanded portion at the 3 cell types in the olfactory mucosa:
tip of the dendrites) 1. Basal cells,
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PHYSIOLOGY: TASTE & SMELL
2. Sustentacular cells (helps to support the  Water soluble
olfactory receptor neuron; serves as a o Penetrates the hydrated mucous
structural and nutritional support for membrane of the nasal epithelium
olfactory neurons), and  Lipid soluble
3. Basal cells o Penetrates phospholipid bilayer of
4. Bowman’s gland (minor cell which secretes olfactory receptor neurons to activate the
mucous) cells.
 Small (3-4 to 18-20 carbon atoms)
The axons of these neurons are TYPE C, so impulses  Different structural configurations give rise to
conducted is very slow, relatively to other afferent different odors
neurons.  So… the more water soluble and lipid soluble the
odorants are, the more the stronger they smell.
Olfactory Bulb
 Location of olfactory glomeruli Odorant Binding Proteins (OBP)
o Axons of olfactory receptors +  Seen within the mucous layer
dendrites of mitral cells and tufted  Concentrate the odorants and transfer them to
cells the receptors.
 Contains periglomerular cells  Accelerates the binding of olfactory molecules to
o Inhibitory neurons connecting one the segment of the polypeptide chain of receptor
glumerolus to another proteins
 Contains granule cells
o Doesn’t have axons There are also electrolytes present, which is responsible
o Makes reciprocal synapses with for the changes in the membrane conductance. All of the
lateral dendrites of mitral cells and receptor potential involves movement of cations into the
tufted cells. membrane during the depolarization process.

Just a clarification…
Classification systems of olfactory stimuli
Cranial nerve I does not comprise the olfactory bulb Odor Class Example of Smells like
and olfactory tract, it is the axons of the olfactory known
receptor neuron which comprise the olfactory bulb compounds
and tract. Floral Geraniol Roses
Ethereal Benzyl acetate Pears
Olfactory neuron cells are not like taste cells, they are Musky Muscone Musk
neurons. The taste cells are specialized epithelial cells. Camphor Cineole, camphor Eucalyptus
Both have short lifespan. Putrid Hydrogen Rotten eggs
sulfide
Pungent Formic acid, Vinegar
acetic acid
Cats and dogs have a strong sense of smell
 Possibly the representation of olfactory receptor This was an attempt by the scientists before to classify the
neuron in the brain of cats and dogs. different olfactory sensations, but sad to say, this was not
 Larger surface area of the mucous membrane enough. Current scientists have come up to about 100 to
 Blessed to have a vomeronasal organ
o Contributes to the regulation of the Fact:
reproductive cycle of other mammals— Pepperminty smell is due to stimulation of nerve fibers.
sensitive to pheromones on the air
released by the opposite sex. 1,000 primary sensation from which those 10,000 odorant
molecules can be identified.
 Contains 230,000,000 olfactory receptor neurons
while in humans, there are only 10 to 20.

Characteristics of olfactory molecules: They bind to olfactory receptor proteins in the cilia of the
olfactory neurons. Current scientists say that this
 Volatile
classification is not enough in classifying a more than
o Transported by air
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PHYSIOLOGY: TASTE & SMELL
10,000 odorant molecules which have already been STIMULUS TRANSDUCTION MECHANISM:
recognized.
Recall that the cilia contain a metabotropic receptor
which is embedded in the phospholipid membrane.
II. RECEPTOR SENSITIVITY AND ADAPTATION These receptor proteins have the ability to bind a wide
OF THE OLFACTORY RECEPTOR NEURON. range of olfactory molecules.

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 Depolarize
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.

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,

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PHYSIOLOGY: TASTE & SMELL
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 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 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 1 st order
Figure 4. IP3 Pathway neuron compared to the 2nd order neuron. In the 2nd order
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 neuron manifests a rapidly adapting response – so we can
some receptors of the ER to open the calcium stores to release calcium, which see that there is a desensitization mechanism because of
helps in depolarizing the cell. the very strong smell. Our CNS has the ability to stop the
barrage of signals so that we won’t be overwhelmed with
In this case, there is no myelin sheath in the olfactory the smell.
receptor neuron because it is a type C, so sa axon hilux or
sa initial segment lang siya nag-gegenerate dahil wala naming Odor B – There is a basal activity in the 1st order neuron
nodes of ranvier. but stops as the impulse reaches the 2 nd order neuron.
Somehow there is still a manifestation of odor signal, so
there can either be a discharge recognized by CNS or an
III. DISCRIMINATION OF ODOR INTENSITY association of discharge because there is a basal activity
AND QUALITY; ODOR STIMULUS in the 1st order neuron.
LOCALIZATION
Odor C: No response for both. So these are just tonic or
resting discharges.
How can the olfactory system discriminate more than
10,000 kinds of odorant molecules?
So this experiment concludes that the Olfactory
Olfactory neurons utilize a large number of G-protein- receptor neurons respond in different ways
coupled receptor molecules to detect a wide range of depending on the molecule. With 3 molecules, they
odors. About 1,000 genes encode and produce 1,000 respond differently.
Olfactory receptor proteins. (About 1 % of Human
genome). There are about 1,000 olfactory receptor cell Please refer to Dr. Simbulan’s handout on Taste & Smell for the diagram
types, each one producing a protein. and for a more in depth discussion regarding adaptation.

Each olfactory receptor proteins bind to an array of these Why can we LOCALIZE source of odor stimuli ?
odorant molecules, which explains why we can
distinguish about 10,000 or more different odors.
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PHYSIOLOGY: TASTE & SMELL
Crude Topographic Representation of Olfactory Receptor can prevent inflow of signals from 1st order
Cells in the olfactory bulb give spatial information about neurons to 2nd order neurons.
stimuli.
Summary:

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

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,
Adaptation mechanisms at the peripheral level: read more on lateral inhibition and descending
inhibition by periglomerular and granule cells in the
(1) Phosphorylation of kinases prevents the olfactory bulb, ―shaping‖ the responses of 2nd-order
interaction of G-protein and portion of neurons.)
polypeptide chain of receptor
 Kinase causes the phosphorylation of Axons of mitral and tufted cells comprise the olfactory
polypeptide chain and therefore will tract. In animals, the vomeronasal organ is connected to
change in conformation. This another pathway. The human olfactory cortex helps in
prevents the access to the binding sensory discrimination of olfactory system.
site of G-protein. The cascade stops
even if the odorant molecule binds to From the olfactory cortex, olfactory information reaches
the receptor. other cortical areas via the thalamus (and hypothalamus).
[Unique to olfaction, note that the thalamus does not
(2) Desensitization of cAMP serve as a relay from receptor to olfactory cortex.]
 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.
Olfactory information, from bilateral sides of olfactory
.
cortex, is also conveyed via the thalamus with greater
Adaptation mechanisms arising from inhibitory signals
projection to and activation of the right side of the
from CNS structures:
orbitofrontal cortex . This is for conscious olfactory
perception and discrimination.
1. Periglumerolar cells and granule cells are
inhibitory neurons and are activated by some
descending inputs from the olfactory cortex. So
5 main areas of the olfactory cortex and functions:
when there is a barrage of strong smells,
ascending inputs can be inhibited by both
1. Anterior olfactory nucleus
ascending and lateral inhibition mechanism. It

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PHYSIOLOGY: TASTE & SMELL
 An integrative center connecting the two 2. Neurological disorders
olfactory bulbs through the anterior such as Parkinson’s and
commissure; integration of olfactory inputs; Alzheimer’s
information-sharing

2. Piriform cortex Any lesions cause anosmia. Age-related changes in smell


 Main area involved in olfactory also occur as a result of decreased number of cells in
discrimination; electrical stimulation in olfactory bulb and nasal lining.
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.

Figure 5. Diagram of the olfactory pathway. Information is transmitted from the olfactory bulb by axons and tufted relay neurons in
5. Part of enthorhinal cortex

the lateral olfactory tract. Mitral cells project to five regions of the olfactory cortex: Anterior olfactory nucleus, olfactory tubercle,
piriform cortex, and parts of the amygdala. Conscious discrimination of odor depends on the neocortex (orbitofrontal and frontal
 Receives olfactory input and projects to
hippocampus;
 Involved in olfactory memories.

Please refer to the diagram on your right so you guys can


fully visualize the areas of the olfactory cortex.

cortices). Emotive aspects of olfaction derive from limbic projections (amygdale and hypothalamus).
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

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PHYSIOLOGY: TASTE & SMELL
PART 2: SENSE OF TASTE a. Anterolateral portion Glossopharyngeal
b. Posterior portion Facial nerve

I. HISTOLOGY/ANATOMY

Taste buds Figure 2. Distribution of taste


 Composed of 50 modified epithelial cells: buds in human oral cavity and its
 Sustentacular corresponding afferent nerves
 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, Tongue Map
epiglottis, proximal esophagus. Areas of the tongue
respond to various taste
 Beyond the age of 45, many taste bids degenerate
stimuli. For decades, there
 There are 40 to 60 cells per taste bud.
was a traditional tongue
 They have a short lifespan (10 days to 14 days),
map which was shown
but are replenished by basal cells.
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
Figure 1. Anatomical features of the taste bud. Each taste bud is made up of 4
 Mainly sensitive to hydrogen containing
types of cells: Basal cells; Type 1 & Type 2 cells (sustentacular cells); Type 3 substances such as Acids (H+).
cells (gustatory receptor cells that make up synaptic connections to sensory  Intensity of the taste is proportional to
nerve fibers); Von Ebner’s gland (secretes mucous mixture that contains the concentration of hydrogen ions. The
proteins).
more acidic the food, the more sour it
gets.
Various taste buds are located in the oral cavity and walls
of pharynx. The oral cavity is innervated by various
2. Salty tasting substances
cranial nerves. Taste buds cell are situated on the
posterior, anterior, lateral portions of the tongue.  Sodium-containing substances (Na+), as
well as some organic compounds (e.g.
Location of taste bud Innervation
lysyltaurine, ornithyltaurine)
Pharyngeal wall Vagus nerve
 Cations of the salts (Na cations) are
Epiglottis Vagus nerve
mainly responsible for the salty taste, but
Palate Facial nerve
anions also do contribute but in a lesser
Tongue
extent.
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PHYSIOLOGY: TASTE & SMELL
Sucrose Sweet 10,000
Saccharin Sweet 23

Figure 3. We have a low threshold for Saccharin (an artificial sweetener),


3. Sweet tasting substances which makes us more sensitive. High threshold means lower sensitivity to
substances and low threshold means higher sensitivity.
 Mostly organic (sucrose, maltose, lactose,
glucose , other polysaccharides; some So basically, substances that are edible and have nutritive
proteins; also lead salts, artificial value have a relatively higher threshold to substances
sweeteners) that are toxic. This is important so that we won’t be
 Slight changes in chemical structure can overwhelmed with the taste of the food, to the extent that
often change the substance from sweet to we might reject or stay away from it. Also, toxic
bitter. substances such as HCl have a low threshold (therefore
high sensitivity) so that we are able to detect it, and
4. Bitter tasting substances therefore it prevents from burning our GIT.
 Organic substances such as morphine,
Nicotine, caffeine, urea; inorganic salts of Saccharin is an artificial molecule and has been
magnesium. Ammonium, and calcium withdrawn from the market. Saccharin was in many
(due to cation). products which are calorie free. Aspartate has replaced
 There are 2 particular class of substances saccharine. It came back. Sometime it was banned from
are especially likely to cause bitter taste: the market because it was carcinogenic.
- Long-chain organic substances
that contain nitrogen We also have low threshold for bitter substances.
- Alkaloids (include many of the  Glycine chloride binding receptor antagonist -
drugs used in medicines such blocks inhibitory neurotransmitter glycine so we
as quinine, caffeine, strychnine, may have convulsion
nicotine)  toxic, use for malaria
 Nicotine - toxic doses if increased sensations.
5. Umami tasting substances
 Taste sensation produced by glutamate Some bitter substances can have antioxidant properties,
and glutamate-like substances, found in but some are toxic. So, bitter taste has higher sensitivity
seaweeds and other seafoods. and low threshold.

Facial nerve is more sensitive to: IV. General transduction Mechanisms by Gustatory
Sugar > Salty and sour > bitter Receptor Cells

Glossopharyngeal nerve is more sensitive to: (1) Interaction of taste stimuli with the apical
Sour and bitter > sweet and salty membrane either by:
 Binding to G-protein coupled receptors
Vagus nerve is more on pharynx  Modulating apically located ion channels
 In regurgitation, we can actually taste it –  There are 13 types of chemical receptor
so it is a somatosensory feeling. It's a real proteins in taste bud cells:
taste sensation when we feel the acid from  2 sodium receptors
our stomach to our pharynx.  2 potassium receptors
 1 chloride receptor
Sensation is also sensitive to water – it is also mapped out
 1 adenosine receptor
as one of the taste stimuli
 1 inosine receptor
 2 sweet receptors
 2 butter receptors
III. Taste Thresholds and Intensity Discrimination
 1 glutamate receptor
 1 hydrogen ion receptor
Substance Taste Threshold
Concentration (μmol/L)
Hydrochloric acid Sour 100
 Primary sensation of taste is used for
Sodium Chloride Salt 2,000
practical analysis of taste, so it can also be
Strychnine Bitter 1.6
grouped into 5 general categories
hydrochloride
 Sour
Glucose Sweet 80,000
 Salty
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PHYSIOLOGY: TASTE & SMELL
 Sweet
 Bitter
 Umami

 Molecular characteristics of receptors:

Taste Ionotropic Metabotropic


Sensation Receptor Receptor (G-
protein coupled)
Salty Yes
Sour Yes
Sweet Yes
Bitter Yes
Umami Yes
MECHANISM FOR SOUR TASTE:

There are no H+ ion channels to which they pass. In this


(2) Generation of Receptor Potential: case, they block potassium channels, which causes
 Change in electrical potential in the taste depolarization.
cell.
 Membrane of taste cell is negatively 2 ways of depolarizing the membrane:
charged on the inside with respect to the 1. Potassium channel is blocked by H+
outside. Application of taste substance to a. There is a build up of positive ions,
the taste hairs causes depolarization. especially if Na-K pump is active, which
 In most cases, the decrease in potential brings potassium more inside and
(therefore decrease in depolarization) is sodium outside.
proportional to the concentration of the
stimulating substance. 2. Entrance of H+ in through ENaC
 Mechanism: a. CNS is the one responsible for giving the
 Binding of taste chemical to taste sensation, not the ENaC. So, ENaC
protein receptor molecule of which is originally seen in the pathway
taste receptor cell for salty substance does not cause the
 Causes the entrance of Na+ salty taste in this area. For every taste
ions or H+ ions  causes sensation, there is a specific cortex which
depolarization is responsible for a specific taste.

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.
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PHYSIOLOGY: TASTE & SMELL
MECHANISM FOR SWEET TASTE: removed, resulting in cation influx.); PDE =
phosphodiesterase; PDE reduces cAMP concentration.
1. Adenylyl cyclase/ cAMP pathway: (receptor = T2R class)

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 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:
MECHANISM FOR BITTER TASTE Activation of a truncated metabotropic
glutamate receptor (mGluR4) in the taste
There may be as many as 24 G-protein-linked bitter buds, with agonists being purine 5-
receptors in humans. Some examples below. ribonucleotides such as IMP and GMP in the
food. Mechanism of depolarization through
1. PLC/ IP3-DAG Pathway: this mechanism unsettled.
Denatonium (bitter-tasting molecule), interacts with a G-
protein-coupled receptor, which activates phospholipase
C (PLC), producing IP3 (2nd messenger). IP3 increases V. DISCRIMINATION OF TASTE QUALITY &
intracellular Ca 2+ levels, leading to release of synaptic INTENSITY
transmitter, and activation of gustatory nerve fiber.

2. Phosphodiesterase activation  Each nerve fiber in the gustatory nerves responds


Denatonium binds to a G-protein (gustducin) - coupled to more than one taste stimuli.
receptor, activating phosphodiesterase, causing a
decrease in cAMP; cAMP block of cation channels is
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PHYSIOLOGY: TASTE & SMELL
 However, each fiber responds best to one of the 3. The third-order neurons
four primary taste qualities. Pass through the internal capsule and terminate in the
region of the ipsilateral postcentral gyrus in the face area
 The coding of a gustatory sensation (taste of the Parietal Cortex . The 3rd order neurons also project
quality) is not a simple, labeled-lined mechanism. to the anterior part of the insular cortex; this area is said
It is a pattern of activities in nerve fibers activated to mediate conscious perception of taste and taste
by a particular stimulus. discrimination ).

 Taste stimulus intensity discrimination is crude, Reflexes are mediated by nucleus tractus solitarius
as it takes a 30% increase in concentration before anterior insula
a difference in taste stimuli intensity is detected.
Note similarity with smell discrimination. Lesions in the anterior insula (foot of postcentral gyrus) -
a. Example: Increasing the salt we lose taste sensation
concentration by another 5%, 10% and
20%, it will remain undetected unless we VIII. DISORDERS OF THE SENSE OF TASTE:
increase it by 30%
1. Ageusia – absence of sense of taste.
2. Hypogeusia – diminished taste sensitivity

VI. TASTE RECEPTOR CELLS EXHIBIT A RAPID


ADAPTATION MECHANISM Short lifespan - taste bud cells are replenished by basal
cells. If basal cells are diminished, there is reduced in the
Adaptation of the gustatory system (almost complete, ability to generate sensor cells thus we lose taste
within a minute or so of continuous stimulation) results sensitivity as we get older. Lifestyle is also a factor.
from:

a. Sensory adaptation (ADAPTATION at the level of the Synthetic sense of flavor:


taste bud cells) The culinary experience is an integration of sensory
inputs: Smell, sight, tactile, thermal, and memory, and
b. Central adaptation (adaptation at the level of higher- even the emotional aspect.
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
END OF TRANSCRIPTION
or changes in response to taste receptors cells. There's
If the diagrams are not clear, please refer to Dr. Simbulan’s handout
always a constant stimuli in our taste bud cells,
regarding Taste & Smell physiology and also to the book of Ganong.
representing various taste. 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
Taste receptor cells are rapidly adapting. 100% passing in the boards! Happy Studying! 

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).

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PHYSIOLOGY: TASTE & SMELL

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