Olfactory and Taste Physiology Primer (1).pdf

OLFACTION The olfactory system is capable of processing information about the identity, concentration, and quality of airborne (volatile) stimuli and it does so because it is organized in a manner where odorants interact with the olfactory epithelial surface receptors directly. Within your nasal muc...

OLFACTION The olfactory system is capable of processing information about the identity, concentration, and quality of airborne (volatile) stimuli and it does so because it is organized in a manner where odorants interact with the olfactory epithelial surface receptors directly. Within your nasal mucosa, olfactory receptor neurons exist that bind specific odorant molecules and transmit olfactory information through their axonal projections to the olfactory bulb. Groups of axons from olfactory receptor neurons within the nasal mucosa epithelium are called olfactory nerves. These nerves project to the olfactory cortex via the olfactory tract where smell is processed. Olfactory receptor neurons (ORNs) are bipolar neurons in the nasal mucosa that exhibit small diameter and unmyelinated axons at their basal surface. At their apical surface (facing the lumen of your nasal cavity), these neurons consist of a single dendritic process that forms a knob-like protrusion extending into olfactory cilia. Olfactory cilia are critical in olfaction since it is the binding of the odorant to receptors on these cilia that is responsible for eliciting changes in membrane current. Stimulation to the cell body of an olfactory neuron has little to no effect. Other structures within the olfactory epithelium include supporting cells, basal cells, precursor stem cells, and developing receptor cells. It is important to recognize that within the olfactory epithelium, ORNs are continuously generated from dividing precursor stem cells. These ultimately develop into mature ORNs that are capable of binding odorants and transmitting olfactory information. Because of the presence of the continuous division, ORNs are turned-over (renewed) every 6-8 weeks. Basal cells and support cells create a suitable environment for these developing and mature ORNs. Specifically, basal cells contain enzymes which degrade and detoxify harmful substances that come into contact with the nasal epithelium. Glandular structures (Bowman’s gland) also exist within this mucosa and serve the purpose of secreting mucous to keep the epithelium moist and allow odorants to solubilize onto receptors. ORNs project their basal axons to the olfactory bulb. Glomeruli within the olfactory bulb receive these excitatory projections from many different ORNs, demonstrating convergence. For example, one glomerulus structure may receive up axons from up to 25,000 ORNs. Glomeruli, in turn, diverge this information onto mitral cells. Each glomerulus will send information to ~25 mitral cells within the olfactory bulb. Mitral cells form the lateral olfactory tract which conveys olfactory information directly to the olfactory cortex. Before we discuss the cortical processing of olfactory information, let’s discuss how the receptors of the ORNs within the nasal epithelium bind and transduce olfactory signals. ORNs have receptors that are G-protein coupled (GPCR). Odorants bind directly to GPCR molecules located in the membranes of the cilia. This association activates an odorant-specific G-protien (Golf) that, in turn, activates adenylate cyclase. This activation results in the generation of cyclic AMP (cAMP) which targets cation-selective channels that permit the influx of sodium and calcium into the cilia, resulting in depolarization. The increase in intracellular calcium opens calcium-gated-chloride channels that provide the depolarization for the olfactory receptor potential. Olfactory Processing From the olfactory tract, olfactory information is sent to the olfactory bulb targets including the piriform cortex (archicortex), olfactory tubercle, amygdala, and entorhinal cortex. It is important to note that olfaction is the one sense that does not require a direct relay through the thalamus. Instead, information from the initial olfactory bulb targets can be distributed to the hippocampus, thalamus, hypothalamus, and frontal cortex for additional processing. Transmission of olfactory information to the hypothalamus and hippocampus can have a direct impact on feeding, reproduction, and aggression while information that is exchanged between the piriform olfactory cortex and orbitofrontal cortex allows individuals the conscious appreciation of odorants and enables one to associate olfactory information with other sensory characteristics. Odorant perception in mammals Although not entirely critical to your understanding of olfactory abilities, it is interesting to note that odorant perception differs across species. For example, the acuity for the sense is directly related to the necessity of that sense for survival and the size of the olfactory bulb and cortex (or area of forebrain devoted to olfaction) is also a result of olfactory necessity. In the example provided below, dogs contain large densities of ORNs that allow them to smell far more substances at far less concentrations than humans could ever hope to. However, in the rat, although the number of ORNs is fairly similar to what we have in our own nasal epithelium, the area of forebrain devoted to olfactory abilities is significantly increased over ours, allowing for a greater ability of rodents to process olfactory. In humans, olfaction is the least acute sense reflected by the fact that we have a reduced number of ORNs and area of forebrain devoted to olfaction. Anosmia and declines in olfactory sensitivity Anosmia is a chemosensory deficit that results in the inability to smell. In general, however, anosmia is usually restricted to a single odorant suggesting that a single element (e.g., odorant receptor gene, receptor, relay) of the olfactory system is comprised. This is normally not a huge issue, though it could become potentially dangerous if the odorant incapable of being transduced is lethal (e.g., toxic gas). Anosmia can also be transient in nature and emerge as a result of chronic sinus infection, inflammation, head injury, or aging. An age-related decline in olfactory sensitivity is normal. Normally, as individuals age, there is a diminished peripheral sensitivity and/or altered activity of CNS olfactory structures. Reductions in olfactory sensitivity can also be a result of neurodegenerative or neuropsychiatric conditions. For example, individuals who suffer from Alzheimer’s disease have significantly diminished olfactory sense whereas individuals who suffer from schizophrenia often exhibit a radically distorted perception of smell. What are the consequences of a decline in olfactory ability? The consequences would be a result of changes to the normal physiological and biological responses to odorants. When we consider odorants, it remains important to recognize that they elicit physiological responses in the form of changes to visceral motor, reproductive, and endocrine function. They are also responsible for generating behavioral responses (e.g., a bond between a mother and child). In addition, though having already been demonstrated to not be the case in humans, odorants promote species-specific interactions through what is termed pheromone signaling. Pheromone signaling plays an important role in establishing and maintaining appropriate social, reproductive, and parenting behaviors among animal species. It is through the action of pheromone signals on specialized receptors within vomeronasal organs (VNO) that this process can occur. The VNO has projections that directly and indirectly connect it to the main olfactory bulb (MOB) and accessory olfactory bulb (AOB). Without a normal olfactory ability, animals would suffer a decline in social and reproductive successes. GUSTATION The human taste system converts the chemical and physical properties of food into electrical signals. In this way, the human taste system is also able to identify the nutritive and/or aesthetic properties of food, along with the safety of it. This occurs through the interaction of solubilized tastants molecules with receptor proteins on taste cells located in the epithelial specializations termed “taste buds” on the tongue. The gustatory (taste) system is heavily innervated by the visceral motor system which allows for the functions of salivation, swallowing, gagging, etc. However, external features of the gustatory system also have an impact on what we eat and like. For example, the texture and temperature of food often plays an important role in how one perceives it, whether pleasing or unpleasing. Additionally, cultural and psychological factors govern what foods we eat, like, or are just plain used to. Signal transduction mechanisms of taste Taste cells are specialized epithelial cells organized into onionshaped units, called taste buds. Each taste buds contains about 50100 taste cells distributed in taste papillae on the surfaces of the tongue, palate, pharynx, and larynx. Taste cells are responsible for stimulus identity and quantity of a tastant, where in most cases the perceived intensity of the stimulus is proportional to the concentration of the stimulus. Taste papillae contain different distributions of taste buds/cells specific for different solubilized molecules, owing to the idea that different areas of the tongue are more sensitive to different types of food (e.g., sweet, salty, sour, etc). Taste cells are composed of two distinct domains. Receptors for different tastants are located in the apical domain of the cell (exposed to the oral cavity). The activation of these receptors introduces ions and second messengers that act on the basal domain of the taste cell. The initial depolarization in the apical domain allows for voltage-gated sodium, calcium and potassium channels within the basal domain to open, allowing for the exocytosis of neurotransmitter onto afferent sensory neurons. Different tastants require the binding to different taste cell receptors in order to transduce their signal and mediate an actual taste (e.g., salty, sweet, sour, umami, bitter). Salt – salt binds to an amiloride-sensitive sodium channel that allows for the influx of sodium and the depolarization of the taste cell. Sour – acids from sour foods bind to proton sensitive cation channels that allow for the influx of protons to depolarize the taste cell. Sweet – sweet foods bind to the T1R2 protein of a GPCR dimer (also consisting of T1R3). This initiates an intracellular signaling cascade leading to the dissociation of -g protein, which subsequently binds to phospolipase C-beta2 (PLC ) leading to the release of IP3 and the opening up of a calcium selective TRPM5 channel. Amino acids – these act in the same manner as sweets, but the amino acids bind a T1R1 GPCR dimer (also consisting of T1R3). Bitter – to transduce bitter tastes, these tastants bind to a GPCR (T2R), initiating the release of the -g protein, gustducin, which acts to cleave PLC into IP3 to activate TRPM5 calcium selective channels. Targets for the human taste system Taste buds relay information through distinct cranial nerves which synapse onto the solitary nucleus of the brainstem (NTS). From the NTS, projections are sent to the insular and frontal cortex for higher order processing and associative learning while other projections extend to the hypothalamus to regulate visceral motor function or the amygdala to regulate the emotional response to tastants. Although not depicted in this diagram, tastant information is also relayed to central motivation and reward centers (remember the ventral tegmental area of the basal ganglia?) where the positive properties of food are reinforced.