Olfaction And Taste
The olfactory or first
cranial nerve contains more fibres than any other sensory nerve projecting to the CNS, while taste is relayed
via the seventh, ninth and tenth cranial nerves (see Chapter 7).
Olfaction
The olfactory system as a whole is
able to discriminate a great diversity of different chemical stimuli or odours,
and this is made possible through thousands of different olfactory receptors.
These receptors are located in the apical dendrite of the olfactory receptor
cell and the axon of this cell projects directly into the central nervous
system (CNS) via the cribriform plate at the top of the nose to the
olfactory bulb.
The olfactory stimulus or odour,
on binding to the olfactory receptor, depolarizes it (see Chapter 23) which, if
sufficient, leads to the generation of action potentials at the cell body which
are then conducted down the olfactory nerve axons to the olfactory bulb.
The olfactory nerve passes
through the roof of the nose through a bone known as the cribriform plate.
Damage to this structure (e.g. head trauma) can shear the olfactory nerve axons
causing a loss of smell or anosmia, although the most common
cause of a loss of smell is local trouble within the nose, usually infection
and inflammation. The olfactory receptor axons then synapse in the olfactory
bulb that lies at the base of the frontal lobe. Damage to this structure, as
occurs in frontal meningiomas, produces anosmia that can be
unilateral.
The olfactory bulb contains
a complex arrangement of cells. The axons from the olfactory nerve synapse on
the apical dendrites of mitral and, to a lesser extent, tufted cells, both of
which project out of the olfactory bulb as the olfactory tract. The olfactory
bulb contains a number of inhibitory interneurones (granule and periglomerular
cells), which are important in modifying the flow of olfactory information
through the bulb. Some of these neurones are replaced throughout life, with the
neural precursor cells for them originating in the subventricular zone and then
migrating to the olfactory bulb via the rostral migratory stream, a structure
that has been shown to exist in the adult mammalian brains including in humans.
This system may be important in olfactory learning.
The olfactory tract projects
to the temporal lobe where it synapses in the piriform cortex and limbic
system, which projects to the hypothalamus. This projection is
important in the behavioural effects of olfaction, which are perhaps more
evident in other species. In humans, lesions in these structures rarely produce
a pure anosmia, but activation of this area of the CNS as occurs in temporal
lobe epilepsy (see Chapter 61) is associated with the abnormal
perception of smells (e.g. olfactory hallucinations).
The projection of the olfactory
system to the thalamus is small and is mediated via the olfactory tubercle to
the mediodorsal nucleus, which projects to the prefrontal cortex. The role of
this pathway is not clear.
Taste
The taste or gustatory
receptors are located in the tongue. They are clustered together in
fungiform papillae with supportive stem cells; the latter dividing to replace
damaged gustatory receptors. The apical surface of the gustatory receptor
contains microvilli covered in mucus, which is generated by the neighbouring
goblet cells. Any ingested compound can therefore reach the gustatory receptor;
hydrophilic substances are dissolved in saliva while lipophilic substances are
dissolved in the mucus. Taste is tradition- ally classified according to four
modalities – salt, sour, sweet and bitter – which correlate well with the
different transduction processes that are now known to exist for these
different tastes. A fifth taste (umami) has also recently been described.
•
Salt
stimuli cause a direct
depolarization of the gustatory receptors by virtue of the fact that Na+
passes through an amiloridesensitive apical membrane channel. The
depolarization leads to the release of neurotransmitter from the basal part of
the cell which activates the afferent fibres in the relevant cranial nerve.
•
Sour
stimuli, in contrast, probably
achieve a similar effect by blocking apical voltage-dependent H+
channels.
•
Sweet
stimuli bind to a receptor
that activates the G protein, gustducin, which then through adenylate cyclase
leads to cyclic adenosine monophosphate (cAMP) production. The rise in cAMP
activates a protein kinase that phosphorylates and closes basolateral K+
channels and by so doing depolarizes the receptor.
•
Bitter
stimuli similarly rely on
receptor binding and G-protein activation. One pathway involves gustducin but,
in this instance, it leads to activation of a cAMP phosphodiesterase, which
reduces the level of cAMP (and so the phosphorylating protein kinase) leading
to opening of the basolateral Ca2+ channels and so transmitter
release. An alternative pathway for both sweet and bitter tastes involves the
activation of a phospholipase C and the production of inositol triphosphate (IP3)
and diacylglycerol (DAG), which can release Ca2+ from internal
stores within the receptor. The increased Ca2+ concentration
promotes neurotransmitter release.
The receptors relay their
information via the chorda tympani (anterior two-thirds of the tongue)
and glossopharyngeal nerve (posterior third of the tongue) to the
nucleus of the solitary tract in the medulla (see Chapters 7 and 8). The
structure projects rostrally via the thalamus to the primary somatosensory
cortex (SmI) and the insular cortex, with a possible additional projection to
the hypothalamus and amygdala. Some patients with temporal lobe epilepsy have
an aura of an abnormal taste in the mouth which may relate to ictal electrical
activity within the temporal lobe (see Chapter 61).
