Hearing and balance
The vestibulocochlear or VIII cranial nerve is composed of two parts - the cochlear nerve, associated with hearing, and the vestibular nerve, associated with maintaining balance and posture. Both auditory and vestibular end organs are located in the inner ear. They have some similarities and, at the same time, critical differences.
Cochlear system: The ear is composed of external, middle, and internal ears. The middle ear is air filled and has a tympanic membrane which separates it from the external ear. The middle ear also has three bony ossicles called malleus, incus, and stapes. The footplate of the stapes inserts into the oval window between the middle and inner ear. The inner ear is fluid-filled. It has a bony and membranous labyrinth. The bony labyrinth comprises three semicircular canals - lateral, posterior, and superior. The membranous labyrinth consists of ducts called scala vestibuli, scala media, and scala tympani. The fluid in the scala vestibuli and tympani is called perilymph and is similar to extracellular fluid. The fluid in the scala media is endolymph and is high in potassium. A spiral structure called the cochlea contains the organ of Corti, which is associated with the perception of sound and hearing. The organ of Corti lies on the basilar membrane. It has two types of ciliated hair cells - inner and outer. The cilia are embedded in the tectorial membrane. Hair cells near the base of the basilar membrane are most sensitive to high frequencies, while those at the apex respond best to low frequencies.
When sound waves hit the eardrum, it vibrates. This moves the chain of ossicles, pushing the footplate of the stapes into the oval window. This displaces the fluid in the inner ear causing vibrations in the organ of Corti which in turn leads to bending of the hair cell cilia. Bending in one direction causes increased potassium efflux and hyperpolarization, while bending in another direction leads to increased potassium influx and depolarization. Depolarization causes increased intracellular calcium levels and release of excitatory neurotransmitters leading to stimulation of the cochlear nerve endings.
Neurons located in the spiral ganglion contribute to the first-order neurons of the auditory pathway. They are bipolar neurons, with shorter axons innervating the hair cells and longer axons reaching the CNS as the cochlear nerve fibres. The cochlear nerve will synapse with ventral and dorsal cochlear nuclei in the medulla, which comprise the second-order neurons of the auditory pathway. Interestingly, from this level onwards fibres connect both ipsilaterally and bilaterally. Some fibers from the ventral cochlear nucleus pass across the midline and synapse with the superior olivary nucleus. These crossing fibres form the trapezoid body. Other fibres synapse with the ipsilateral superior olivary nucleus. Fibres from the superior olivary nucleus will ascend to the inferior colliculus. Fibres from the dorsal cochlear nucleus ascend in the ipsilateral lateral lemniscus. The lateral lemniscus receives ipsilateral as well as bilateral fibres. It synapses with the superior colliculus and medial geniculate body of the thalamus. Fibres from the thalamus project to the primary auditory cortex in the superior transverse temporal gyrus located near the lateral or Sylvian fissure.
Due to characteristic bilateral innervation of the auditory pathways in the CNS, unilateral lesions of the CNS do not cause deafness, while local cochlear lesions can cause ipsilateral deafness.
Vestibular system: The receptors of the vestibular system are located in the semicircular canals and otolith organs of the inner ear. There are three semicircular canals, horizontal, superior, and posterior, which are arranged perpendicular to each other. They are involved in detecting the head’s angular or rotational acceleration. The otolith organs are utricle and saccule, which detect linear acceleration or gravitational forces. The semicircular canals and otolith organs are filled with endolymph and surrounded by perilymph.
Vestibular hair cells have special cilia called kinocilium (single, thick cilium) and a bunch of smaller stereocilia. Hair cells are located in the dilated ampulla at one end of the semicircular canal, surrounded by a gelatinous cupula. Together they are called crista. Hair cells are also located within the utricle and saccule where they are surrounded by a gelatinous otolith mass.
The horizontal canals respond to lateral movement of the head, e.g., when the head turns sideways. The superior and posterior canals respond to vertical head movements when the head moves up and down. When the head rotates to the left, it excites (depolarizes) the left semicircular canals and inhibits (hyperpolarizes) the right semicircular canals. Movement of the head causes the gelatinous cupula to move, thus bending the cilia on the hair cells. If the stereocilia bend towards the kinocilium, it depolarizes the hair cell. If the stereocilia bend away from the kinocilium, the hair cell hyperpolarizes.
Similarly, movement of the otolith mass over the hair cells in the utricle and saccule causes bending of the cilia. The mechanism that follows is just like in the semicircular canals.
The neurons of the vestibular nerve are bipolar and are located in the vestibular (Scarpa’s) ganglion. Fibres synapse with vestibular nuclei in the medulla. Medial and superior vestibular nuclei receive inputs from the semicircular canals and relay to the nuclei of cranial nerves III, IV, and VI through the medial longitudinal fasciculus. Lateral vestibular nuclei receive inputs from the utricles and relay them to the motor neurons in the spinal cord via the vestibulospinal tract. The inferior vestibular nucleus receives input from semicircular canals, utricle, and saccule and relays via the medial longitudinal fasciculus to the cerebellum and the brainstem. The lateral and superior vestibular nuclei project to the ventral posterior nuclei of the thalamus. Projections from the thalamus end in the vestibular cortex, also called the parieto-insular cortex. It is under MCA supply.
Olfaction
Odorant chemicals activate olfactory receptors on the nasal epithelium. Olfactory receptors are primary afferent neurons. The receptor proteins are present in the cilia. More than 1000 types of receptor proteins are present. They are GPCR, which activates adenylyl cyclase, causing a rise in cAMP. This opens sodium channels, leading to sodium influx and the receptor cell membrane depolarization. This generates action potentials which are carried along the olfactory nerve. Axons forming the olfactory nerve are small and unmyelinated. They traverse the cribriform plate at the base of the skull and reach the olfactory bulb. The olfactory bulbs lie at the inferior aspect of the frontal lobes. The mitral cell in the olfactory bulb receives input from approximately 1000 olfactory receptor axons, forming a glomerulus-like structure. The mitral cell is the second-order neuron of the olfactory pathway. Nerve fibres from the mitral cells form the olfactory tract that projects to the cerebral cortex. It divides into a medial tract that synapses in the anterior commissure and contralateral olfactory bulb and a lateral tract that ends in the primary olfactory cortex, also known as the piriform cortex. The piriform cortex is located inferomedially at the junction of the frontal and temporal lobes, near the entorhinal cortex. It is a well-known site of origin of focal epilepsy (temporal lobe epilepsy) characterized by olfactory aura.
Taste
Taste receptors are present on the taste buds or papillae. Fungiform papillae on the tip of the tongue detect salty, sweet, and umami taste; foliate papillae on the sides of the tongue detect mainly sour taste, while circumvallate papillae on the posterior tongue detect bitter taste mainly. Bitter substances activate GPCR which leads to increased IP3 and DAG leading to opening of transient receptor potential or TRP channels that cause depolarisation. Sweet and umami act through a similar mechanism but use a different GPCR. Sour substances have H+, which closes K channels on the receptor, causing depolarization. Salty substances have Na, which enters through Na channels directly, causing depolarization. Depolarization causes generation of action potentials in the nerve fibres innervating the taste receptors. Anterior ⅔ of the tongue is innervated by the facial nerve, posterior ⅓ by the glossopharyngeal nerve, posteriormost tongue, and epiglottis by the vagus nerve. So, bitter taste is sensed by the vagus nerve, and so on. The afferent fibres from these three nerves will ascend as the tractus solitarius in the ipsilateral brainstem and synapse with the nucleus of the tractus solitarius in the medulla, which form the second-order neurons of the gustatory pathway. Fibres arising from them project to the VPM nucleus of the thalamus, which then connect to the gustatory cortex located in the insula and inferior frontal gyrus.
