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).
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.
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).