smell Flashcards
describe the olfactory apparatus
Olfactory neurons extend olfactory cilia into the mucous layer which pick up odorants that come in contact with the respiratory epithelium.
Olfactory Receptor Neurons (ORN’s) are continually replaced every 30- 60 days from the basal stem cell population.
Olfactory receptor neurons send up axons through the cribriform plate into the olfactory bulb. And make excitatory synpases (glutamate)
There they form glomeruli which synapse with the mitral and tufted cells which send axons down the lateral olfactory tract to the olfactory cortex
Some can send collaterals to the Anterior olfactory nucleus.
Final destinations:
1. to contralalteral olfactory bulb (anterior commissure & medial olfactory stria)
- to olfactory areas, piriform cortex, olfactory tubercle, amygdala
- these can then end up in hypothalamus, thalamus, hippocampal formation, orbitofrontal cortex
Why is olfaction loss (anosmia) a common sign of Alzheimers
Loss of AON, granule or periglomerular neurons may be responsible for impaired olfaction in AD (these derive from the anterior subventricular zone and are generated throughout life).
Describe odorant receptors
7 transmembrane (7-TM)
ORs are (heterotrimeric) G-protein coupled receptors.
Alpha subunit is specific to ORNs.
•Odorant binding elicits increase in intracellular cAMP levels
•Elevated cAMP stimulates opening of cation channels, leading to depolarization
•Desensitization: In Olfactory Sensory Neurons, activated signal transduction molecules are targeted for negative feedback regulation
Describe the olfactory bulb inputs
Axons of thousands of ORNs expressing the same OR converge at a single glomerulus.
•A single glomerulus reflects the summed activity of all ORNs that express a single OR.
•This convergence is thought to increase the sensitivity of the olfactory system and enhances the signal sent to the brain for activity at each receptor.
•5-25 mitral cell dendrites innervate a single glomerulus.
Concept of olfactory thresholds?
ORN’s exhibit distinct thresholds for particular odorants, suggesting the perception of an odor can change as a function of its concentration.
e.g., [indole]low = floral [indole]high = putrid
Neural encoding of olfactory information
ORs recognize different features of odorants (colors & shapes).
- Odor recognition depends on which receptors are activated and how strongly
- Array of receptor activation leads to unique pattern of glomeruli activation that is consistent between individuals.
- The patterns of activity in the olfactory bulb are transmitted to higher brain regions for processing.
Primary causes of olfactory dysfunction
Primary
•Nasal/sinus diseases: intranasal polyposis, chronic rhinitis,
allergic rhinitis, upper respiratory (viral) infections (common cold)
•Occlusion: Deviated septum, tumors
•Head (cranio-facial) trauma (olfactory nerve shearing)
posttraumatic anosmia as a clinical sign of orbitofrontal damage
- Smoking
- Toxic exposure
- Genetic: specific anosmias (lower sensitivity to a specific
What are secondary causes of loss of smell.
Endocrine: adrenal cortical insufficiency, diabetes mellitus,
Kallmann syndrome, Turner syndrome.
•Neurological: Alzheimer’s, Parkinson’s, Huntington’s chorea.
These disorders often manifest themselves earlier in the olfactory system, perhaps because its actively dividing neurons are more susceptible.
•Cancer therapies: Both chemotherapy and radiation treatments target dividing cells and therefore also have dramatic effects on chemosensory stem cells. Resulting smell and taste deficits are usually temporary, however, presumably because a sufficient number of stem cells remain to allow sensory neuron regeneration.
Conductive
Sensorineural
Conductive losses: Losses secondary to obstruction of the nasal airflow to the olfactory cleft.
Examples include chronic rhinosinusitis (CRS), allergic rhinitis, polyps, and tumors.
Sensorineural losses: Losses secondary to damage to or dysfunction of the olfactory nerves anywhere from the olfactory receptors through the olfactory bulb to the processing centers in the brain.
Examples include loss of smell after upper respiratory infection (URI), head trauma, toxins, congenital disorders, dementia, Alzheimer’s disease, and multiple sclerosis.
Unilateral vs bilateral anosmia
Damage to the olfactory epithelium, the olfactory nerve, the olfactory bulb or olfactory tract can cause unilateral anosmia.
- Destruction of olfactory cortex or olfactory pathways posterior to the trigone (where the tracts divide) must be bilateral to affect olfactory function.
- Ipsilateral anosmia can be difficult to detect due to compensation by contralateral nostril. To perform unilateral testing, occlusion of the non-tested nostril is recommended to prevent crossing of inhaled or exhaled air to the opposite side.
There is a lateral olfactorty stria but also another which is medial olfactory stria that project interneurons allowing the two to communicate with each other. You can envision a unilateral problem or a bilateral problem.
Also medial olfactory strai that interconnect the olfactory bulbs.
So this is important because you can have a unilateral problem or bilateral problem. Unilateral would have to arise anterior to when the tract splits into medial and lateral portions where information can be shared.
It is difficult to assess unilateral or bilateral. IT is not easy to and want to be specific to look for unilateral anosmia.
The three distinct lingual papillae
Three morphologically distinct lingual papillae exist:
-Fungiform (anterior 2/3) comprise 25% of total.
- Circumvallate (posterior 1/3) comprise 50%.
- Foliate (posterior edges) comprise 25%.
What are the CNS connections for taste in the tongue
Anterior 2/3
- CN VII/Facial nerve
- chorda tympani branch
- geniculate ganglion
•Posterior 1/3 -CN IX/Glossopharyngeal -lingual branch -petrosal (or inferior glossopharyngeal) ganglion
•Epiglottis, posterior pharynx
CN X/Vagus
-sup. laryngeal branch
-inferior (nodose) vagal gangion
To the nucleus solitarius
then to the VPM of thalamus
then to the gustatory cortex (insula)
OR
frontal operculum
Taste cells
Taste cells are electrically excitable and can generate action potentials, although they are non-neuronal.
•Taste cell activity is relayed via sensory neurons that innervate them at their basal poles.
Na+, K+ (salty) and H+ (sour) act directly on ion channels, while bitter, sweet and umami tastants act via G-protein mediated intracellular second messenger cascades.
Taste adaptation
- Taste receptors also adapt to the ongoing presence of a stimulus, although the mechanisms are not understood.
- If a chemical is left on the tongue for a sufficient time, it ceases to be perceived (consider saliva, for example).
- Thus, to obtain the full taste of foods, one must either frequently change the types of foods placed in the mouth or wait a sufficient time between helpings (this has long been appreciated by chefs and gourmets).
What is trigeminal chemoreception
Trigeminal chemoreception:
Functions in noxious stimuli detection (nociception) (general somatic). - (spinal component)
•Stimulate polymodal nociceptive fibers.
•Activated by chemical irritants that come in contact with the face or oral cavity.
•Common irritants:
-sulfur dioxide (air pollutant) -ascetic acid (vinegar) -CO2 (in soda) -methanol and ethanol -ammonia (smelling salts) -capsaicin (chili peppers)
•Exposure triggers a variety of responses, including increased salivation, tearing, sweating, decreased respiratory rate, broncho-constriction. These function to dilute the irritant stimulus and reduce further intake.
