TASTE AND SMELL

Smell and Taste are generally classified as visceral senses because of their close
association with the gastrointestinal function. Physiologically they are related to
each other. The flavors of various foods are in large part a combination of their
taste and smell. Consequently, food usually taste different if one has cold that
depresses the chemoreceptor that are stimulated by molecules in solution mucus
in the nose and saliva in the mouth. However these two senses are anatomically
different. The smell receptors are distance receptors (teleceptors), and the smell
pathways have no relay in the thalamus. The taste pathways pass up the
brainstem to the thalamus and project to the post central gyrus along with those
for touch and pressure sensibility from the mouth.

OLFACTION
Olfaction, also known as olfactics, is the sense of smell. This sense is mediated by
specialized sensory cells, called olfactory receptors, in the nasal cavity of
vertebrates that are analogous to sensory cells in the antennae of invertebrates.
In humans, olfaction – the detection of smells – occurs when odorant molecules
bind to specific sites on these receptors. These receptors come together at the
glomerulus, a structure that transmits signals to the olfactory bulb (a brain
structure located directly above the nasal cavity and below the frontal lobe).
Many vertebrates, including most mammals and reptiles, have two distinct
olfactory systems the main olfactory system, and the accessory olfactory system
(used mainly to detect pheromones). For air-breathing animals, the main
olfactory system detects volatile chemicals, and the accessory olfactory system
detects fluid-phase chemicals. Olfaction, along with taste, is a form of
chemoreception. The chemicals that activate the olfactory system, generally at
very low concentrations, are called odorants. Although taste and smell are
separate sensory systems in land animals, water-dwelling organisms often have
one chemical sense.
Volatile small molecule odorants, non-volatile proteins, and non-volatile
hydrocarbons may all produce olfactory sensations. Some animal species are able
to smell carbon dioxide in minute concentrations.
once they activate the sensory
neurons in the nasal cavity? To
get to the brain, the axons of the
olfactory sensory neurons must
get through the skull .
The olfactory epithelium lines the
bone of the part of the skull just
above the nasal passages, and the
axons of the neurons pass directly
through tiny holes in this bone.
Here they enter the first relay
station, the olfactory bulbs, one
on either side of the bottom
surface of the brain (Figure 2,
right).
The electrical signal generated
when an olfactory sensory neuron
is activated is passed along to a
secondary neuron residing in the
bulb,
and from here the signal goes by
way of the olfactory tract to other
brain areas.
 Summary of olfactory pathways.

From the olfactory bulbs, odor

messages go to several brain
structures that make up the
"olfactory cortex,
These areas have connections to the
limbic system (including the
hippocampus, amygdala and
hypothalamus), which is important
in emotional states and in memory
formation.
Thus, a smell frequently activates
intense feelings and memories
before a person even identifies the
odor.
Messages also go to conscious
cortical areas. After a relay in the
olfactory cortex , signals enter a way
station called the thalamus, and
then travel on to the frontal cortex,
where identification and other
related thought processes take
place.

OLFACTORY RECEPTORS/ STEPS OF THE OLFACTORY PATHWAY

The olfactory receptors are embedded in a specialized patch of yellow-tinted

mucus membrane in the roof of the nasal cavity. These receptors are bipolar
neurons covered with modified, non motile cilia. This cilium probably contains
active site for olfactory transduction process. Axons from the olfactory receptors
enter small nerve bundles (collectively termed first cranial nerve) which pass
through the perforations in the cribiform plate of the ethmoid bone and promptly
enter the olfactory bulb.

Olfactory bulb projections

Olfactory sensory neurons project axons to the brain within the olfactory nerve,
(cranial nerve I). These nerve fibers, lacking myelin sheaths, pass to the olfactory
bulb of the brain through perforations in the cribriform plate, which in turn
projects olfactory information to the olfactory cortex and other areas. The axons
from the olfactory receptors converge in the outer layer of the olfactory bulb
within small (~50 micrometers in diameter) structures called glomeruli. Mitral
cells, located in the inner layer of the olfactory bulb, form synapses with the
axons of the sensory neurons within glomeruli and send the information about
the odor to other parts of the olfactory system, where multiple signals may be
processed to form a synthesized olfactory perception. A large degree of
convergence occurs, with 25,000 axons synapsing on 25 or so mitral cells, and
with each of these mitral cells projecting to multiple glomeruli. Mitral cells also
project to periglomerular cells and granular cells that inhibit the mitral cells
surrounding it (lateral inhibition). Granular cells also mediate inhibition and
excitation of mitral cells through pathways from centrifugal fibers and the
anterior olfactory nuclei. Neuromodulators like acetylcholine, serotonin and
norepinephrine all send axons to the olfactory bulb and have been implicated in
gain modulation, pattern separation, and memory functions, respectively.
The mitral cells leave the olfactory bulb in the lateral olfactory tract, which
synapses on five major regions of the cerebrum: the anterior olfactory nucleus,
the olfactory tubercle, the amygdala, the piriform cortex, and the entorhinal
cortex. The anterior olfactory nucleus projects, via the anterior commissure, tos
the contralateral olfactory bulb, inhibiting it. The piriform cortex has two major
divisions with anatomically distinct organizations and functions. The anterior
piriform cortex (APC) appears to be better at determining the chemical structure
of the odorant molecules, and the posterior piriform cortex (PPC) has a strong
role in categorizing odors and assessing similarities between odors (e.g. minty,
woody, and citrus are odors that can, despite being highly variant chemicals, be
distinguished via the PPC in a concentration-independent manner). The piriform
cortex projects to the medial dorsal nucleus of the thalamus, which then projects
to the orbitofrontal cortex. The orbitofrontal cortex mediates conscious
perception of the odor. The three-layered piriform cortex projects to a number of
thalamic and hypothalamic nuclei, the hippocampus and amygdala and the
orbitofrontal cortex, but its function is largely unknown. The entorhinal cortex
projects to the amygdala and is involved in emotional and autonomic responses
to odor. It also projects to the hippocampus and is involved in motivation and
memory. Odor information is stored in long-term memory and has strong
connections to emotional memory. This is possibly due to the olfactory system's
close anatomical ties to the limbic system and hippocampus, areas of the brain
that have long been known to be involved in emotion and place memory,
respectively.
Since any one receptor is responsive to various odorants, and there is a great deal
of convergence at the level of the olfactory bulb, it may seem strange that human
beings are able to distinguish so many different odors. It seems that a highly
complex form of processing must be occurring; however, as it can be shown that,
while many neurons in the olfactory bulb (and even the pyriform cortex and
amygdala) are responsive to many different odors, half the neurons in the
orbitofrontal cortex are responsive to only one odor, and the rest to only a few. It
has been shown through microelectrode studies that each individual odor gives a
particular spatial map of excitation in the olfactory bulb. It is possible that the
brain is able to distinguish specific odors through spatial encoding, but temporal
coding must also be taken into account. Over time, the spatial maps change, even
for one particular odor, and the brain must be able to process these details as
well.
Inputs from the two nostrils have separate inputs to the brain, with the result
that, when each nostril takes up a different odorant, a person may experience
perceptual rivalry in the olfactory sense akin to that of binocular rivalry.

ACTIVATION OF THE OLFACTORY PATHWAY

The binding of the ligand (odor molecule or odorant) to the receptor leads to an
action potential in the receptor neuron, via a second messenger pathway,
depending on the organism. In mammals, the odorants stimulate adenylate
cyclase to synthesize cAMP via a G protein called Golf. cAMP, which is the second
messenger here, opens a cyclic nucleotide-gated ion channel (CNG), producing an
influx of cations (largely Ca2+ with some Na+) into the cell, slightly depolarising it.
The Ca2+ in turn opens a Ca2+-activated chloride channel, leading to efflux of Cl−,
further depolarizing the cell and triggering an action potential. Ca 2+ is then
extruded through a sodium-calcium exchanger. A calcium-calmodulin complex
also acts to inhibit the binding of cAMP to the cAMP-dependent channel, thus
contributing to olfactory adaptation.
This mechanism of transduction is somewhat unusual, in that cAMP works by
directly binding to the ion channel rather than through activation of protein
kinase A. It is similar to the transduction mechanism for photoreceptors, in which
the second messenger cGMP works by directly binding to ion channels, suggesting
that maybe one of these receptors was evolutionarily adapted into the other.
There are also considerable similarities in the immediate processing of stimuli by
lateral inhibition.
Adaptation, or fatigue,
Adaptation involves mechanisms at the level of the receptor cell,
including the inactivation of ion channels in the membrane that
generate the electrical signal.
In a simplified explanation, after a stimulus causes a receptor cell
to produce an electrical signal, the cell membrane soon stops
allowing ions to flow, thus preventing further signals.
Removal of the stimulus followed by restimulation activates the
process all over again.
Researchers have noted that people adapt to odors, such as the
smell of tobacco smoke in a room, more quickly than the
properties of olfactory receptor cells would predict.
Thus, they believe that olfactory fatigue involves some types of
central nervous system mechanisms as well as receptor
adaptation.
 Genes determine the kinds of odor receptors that we have, and
experiences shape our perceptions

Olfactory abilities vary widely among individuals .

There are some people who are able to smell things when no one
else can,
or some who doesn't seem to mind an unpleasant odor when most
people do.
Studies have shown that people who are unable to smell one or one
class of odors frequently have small genetic differences from the
general population.
The inability to smell is called "anosmia," and it may be general, or
specific for one odor.
Temporary general anosmia or "hyposmia" (lessened sense of smell)
can result from a cold or certain medicines.
"Hyperosmia," a heightened sense of smell, can be a genetic trait.
 Olfactory disorders
While genetic differences account for some cases of
anosmia or other olfactory disorders,
most are caused by illnesses or accidents.
Small growths in the nasal cavities (polyps), dental
problems, hormonal disturbances, or sinus infections, as
well as common colds, may cause chemosensory losses.
Injury to the head may damage nerve fibers or break
axons.
Patients who receive radiation therapy for cancers of the
head or neck often develop changes in their sense of smell.
TASTE
In mammals, taste buds are groups of 30-100 individual elongated
"neuroepithelial" cells (50-60 microns in height, 30-70 microns in width), which
are often embedded in special structure in the surrounding epithelium, termed
papillae. In humans the taste buds are located in the mucosa of the epiglottis,
palate and pharynx and in the walls of the fungiform and vallate papillae of the
tongue. At the apex of the taste bud, microvillar processes protrude through a
small opening, the taste pore, into the oral milieu. Just below the taste bud apex,
taste cells are joined by tight junctional complexes that prevent gaps between
cells. Food molecules cannot therefore squeeze between taste cells and get into
the taste bud.
Taste papillae can be seen on the tongue as little red dots, or raised bumps,
particularly at the front of the tongue. These ones are actually called "fungiform"
papillae, because they look like little button mushrooms. There are three other
kinds of papillae, foliate, circumvallate and the non-gustatory filiform. Taste buds,
on the other hand, are collections of cells on these papillae and cannot be seen by
the naked eye. Each taste bud is innervated by about 50 nerve fibers and
conversely each nerve fiber receives input from an average of five taste buds. The
basal cells arise from the epithelial cells surrounding the taste bud. They
differentiate into new ones and the old receptor cells are continuously replaced
with a half time of about 10days.
The sense of taste affords an animal the ability to evaluate what it eats and
drinks. At the most basic level, this evaluation is to promote ingestion of
nutritious substances and prevent consumption of potential poisons or toxins.
There is no doubt that animals, including humans, develop taste preferences. That
is, they will choose certain types of food in preference to others.
Interestingly, taste preference often changes in conjunction with body needs.
Similarly, animals often develop food aversions, particularly if they become ill
soon after eating a certain food, even though that food was not the cause of the
illness - surely you have experienced this yourself. Food preferences and
aversions involve the sense of taste, but these phenomena are almost certainly
mediated through the central nervous system.

Fungiform papillae are located on the most anterior part of the tongue and
generally contain one to several taste buds per papilla. They are innervated by the
chorda tympani branch of the facial (Vllth cranial) nerve. They appear as red spots
on the tongue - red because they are richly supplied with blood vessels. The total
number of fungiform papillae per human tongue is around 200. Papillae at the
front of the tongue have more taste buds (1-18) compared to the mid-region (1-
9). It has been calculated that there are 1120 fungiform taste buds per tongue.
Foliate papillae are situated on the edge of the tongue slightly anterior of the
circumvallate line. They are predominantly sensitive to sour tastes. Innervated by
the glossopharyngeal (lXth cranial) nerve. On average 5.4 foliate papillae per side
of the tongue, 117 taste buds per foliate papillae, total = 1280 foliate taste buds
per tongue.
Circumvallate papillae are sunken papillae, with a trough separating them from
surrounding wall. The taste buds are in tiers within the trough of the papillae.
They are situated on the circumvallate line and confer sour/bitter sensitivity to
the posterior 2/3 of the tongue. Innervated by the glossopharyngeal (lXth cranial)
nerve. 3-13 circumvallate papillae per tongue with 252 taste buds per papillae,
total = 2200 circumvallate taste buds per tongue.
TASTE TRANSDUCTION

Salt taste

Salt is sodium chloride (Na+ Cl-). Na+ ions enter the receptor
cells via Na-channels. These are amiloride-sensitive
Na+ channel (as distinguished from TTX-sensitive
Na+ channels of nerve and muscle). The entry of Na+ causes
a depolarization, Ca2+ enters through voltage-sensitive
Ca2+ channels, and transmitter release occurs and results in
increased firing in the primary afferent nerve.
TASTE RECEPTORS

A very large number of molecules elicit taste sensations through a rather small
number of taste receptors. Furthermore, it appears that individual taste receptor
cells bear receptors for one type of taste. In other words, within a taste bud,
some taste receptor cells sense sweet, while others have receptors for bitter,
sour, salty and umami tastes. Much of this understanding of taste receptors has
derived from behavioral studies with mice engineered to lack one or more taste
receptors.
The pleasant tastes (sweet and umami) are mediated by a family of three T1R
receptors that assemble in pairs. Diverse molecules that lead to a sensation of
sweet bind to a receptor formed from T1R2 and T1R3 subunits. Cats have a
deletion in the gene for T1R2, explaining their non-responsiveness to sweet
tastes. Also, mice engineered to express the human T1R2 protein have a human-
like response to different sweet tastes. The receptor formed as a complex of T1R1
and T1R3 binds L-glutamate and L-amino acids, resulting in the umami taste.
The bitter taste results from binding of diverse molecules to a family of about 30
T2R receptors. Sour tasting itself involves activation of a type of TRP (transient
receptor potential) channel. Surprisingly, the molecular mechanisms of salt taste
reception are poorly characterized relative to the other tastes.