Olfactory Receptors: Location and Structure

The process of olfaction, also known as the sense of smell, is a sophisticated chemical response system. The specialized sensory neurons that facilitate this process, known as olfactory receptor neurons, are situated in an upper segment of the nasal cavity, known as the olfactory epithelium. Olfactory sensory neurons are bipolar, with their dendrites extending from the epithelium's apex into the mucus that lines the nasal cavity. Airborne molecules, when inhaled, traverse the olfactory epithelium, dissolving into the mucus. These molecules, called odorants, bind to specific proteins that maintain their mucus solubility and aid in their transport toward the olfactory dendrites. The odorant-protein complexes bind to receptor proteins within the olfactory dendrites' cellular membrane. The receptor proteins are G protein–coupled and generate a graded membrane potential in the olfactory neurons.

The olfactory neuron's axon originates from the epithelial layer's basal surface, traversing an olfactory foramen in the ethmoid bone's cribriform plate and then projects into the brain. The collection of these axons, termed the olfactory tract, interfaces with the olfactory bulb on the frontal lobe's ventral surface. As a result, these axons bifurcate, undertaking diverse paths to various brain locales. Some axons converge on the cerebrum, particularly the primary olfactory cortex in the temporal lobe's inferior and medial regions. Conversely, other target structures are nested within the limbic system and hypothalamus, facilitating the linkage of odors with enduring memory and emotional reactions. An example of this phenomenon is the evocation of emotional recollections by certain scents, such as the aroma of food native to one's place of origin. Notably, olfaction is the singular sensory modality bypassing a synapse in the thalamus before interfacing with the cerebral cortex. This profound interconnection between the olfactory system and the cerebral cortex elucidates why odors can serve as formidable catalysts for memory and emotion.

The respiratory epithelial tissue, including olfactory neurons, may be susceptible to damage from noxious airborne substances. Consequently, olfactory neural cells within the respiratory epithelium undergo periodic regeneration, during which the axons of the newly formed neurons must establish suitable connections within the olfactory bulb. These emerging axons guide their growth pathway by following existing axons in situ within the cranial nerve.

Anosmia: The Impairment of Olfactory Function

The olfactory nerve, pivotal for the perception of smell, may witness a degradation or a complete loss due to severe facial trauma, a scenario frequently observed in vehicular accidents. This particular affliction is referred to as 'anosmia.' The relative movement of the frontal lobe and the ethmoid bone could result in the severing of olfactory tract axons. Individuals engaged in professional combat sports are often susceptible to anosmia due to constant facial and cranial injuries. Moreover, certain medications, notably antibiotics, have the potential to induce anosmia through the extermination of all olfactory neurons simultaneously. The absence of axons within the olfactory nerve implies that the axons from newly generated olfactory neurons lack a pathway to their respective connections in the olfactory bulb. Anosmia can also be transient due to inflammation resulting from respiratory infections or allergies.

Anosmia can diminish the gustatory experience by rendering food tasteless. Individuals with compromised olfactory capacity may necessitate augmented levels of spices and seasonings to detect flavor in their food. There is a potential link between anosmia and mild depressive states, as the diminished pleasure derived from food could potentially instigate a pervasive sense of melancholy.

The olfactory neurons' regenerative capacity diminishes, leading to age-associated anosmia. This can elucidate the heightened use of salt among older adults compared to younger individuals. However, escalated sodium consumption can augment blood volume and arterial pressure, subsequently escalating the probability of cardiovascular diseases among the older demographic.