Flashcards in 09 16 2014 Chemosensation Deck (22):
detection of volatile compounds (odorants) by the olfactory epithelium of the nose.
-can detect man-made chemicals
lost or impaired smell
risk factors for losing smell?
-higher risk for toxic eposes
-negative impact on life : can't enjoy food or pleasant fragrances.
-associated with other diseases/conditions
Olfactory epithelium (composition of cells in this area)
-Olfactory Receptor Neurons (ORN)
-7 transmembrane G-protein coupled receptor
-alpha subunit is specific to ORNs
-olfactory knob and olfactory cilia -- site of signal transduction due to odor
-basal stem cell population -- 30-60 days
-Bowman's gland = mucus-- allows detection of odor.
-mitral and tufted cell project fibers along olfactory tract. Mitral --> glomerulus of olfactory
Glomerulus of Olfactory epithelium
a single input goes into glomerulus put many neurons from regions can come to that glomerulus if the input matches up.
Glomerulus sums activity of all ORNs that express that single olfactory receptor
Primary causes of olfactory dysfunction?
1. Nasal/sinus disease
3. Head trauma (cranio-facial)
5. Toxic exposure
6. Genetic -- specific anosmias
Secondary causes of olfactory dysfunction
1. Endocrine: adrenal cortical insufficiency, Kallmann syndrome
2. Neurological: Alzheimer's, Parkinson's, Hunginton' chorea
3. Cancer therapies - chemotherapy and radiation
Conductive loss of smell?
losses secondary to obstruction of the nasal airflow to the olfactory cleft.
-chronic rhinosinusitis, polyps
Sensorineural loss of smell?
losses secondary to damage to or dysfunction of the olfactory nerves anywhere from th olfactory receptors through the olfactory bulb to processing in brain centers.
Unilateral anosmia is caused by what?
Damage to olfactory epithelium, olfactory nerve, olfactory bulb OR olfactory tract causes what type of anosmia?
kallmann syndrome (KS)
(heterogeneous) congenital and irreversible form of hypogonadotropic hypogonadism (HH) associated with anosmia
-symptoms present at puberty
-both olfactory receptor neurons and GnRH come from olfactory placode
direct contact of water-soluble compounds with tongue papillae
* olfaction is much more sensitive than taste
Five primary tate qualities/modalities?
salty (ion channel -- Na+ or K+)
sour (protons- through Na+ or K+ channels)
Anatomy of taste (type of taste buds)
Circumvallate papillae (back of tongue - posterior 1/3)
Foliate papilla -- side of tongue
Fungiform papillate - anterior 2/3 of tonuge
Where are taste buds?
open onto the epithelial surface via a taste pore
embedded in papillae of lingual epithelium and in the oral cavity
non-neuronal but they are excitable
-different modalities have different thresholds
Central pathway mediating taste?
1. Anterior 2/3
-CN 7 -- chorda tympani branch
2. Posterior 1/3
- CN9 --lingual branch
Petrosal (inferior glossopharyngeal ganglion)
3. Epiglottis, posterior pharynx
- CN 10 - sup. laryngeal branch
inferior (nodose) vagal ganglion
All go through gustatory nucleus -- nucleus of solitary tract --> ventral posterior medial nucleus of thalamus to cortex
Gustatory cortex? (where?)
-Frontal operulum and insula
What are the two models for neural encoding of taste?
1. Labeled Line code : taste information is transmitted via specific receptors or cells which are tuned to particular qualitities of stimuli
2. Ensemble coding: pattern of responses to a particular stimulus which varies across receptors/cells.
What receptors (modalities) adapt to ongoing presence of a stimulus?
taste and smell
why is it hard for a patient to have a true gustatory disorder?
because 80% of a meal's flavor is a result of olfactory input.
Patients frequently interpret a loss of smell as a loss of taste.
trigeminal chomoreception system?
functions in noxious stimuli detection (nocicieption)
-polymodal nociceptive fivers
-activated by chemical irritants that come into contact with the face or oral cavity.
-trigeminal nerve innervates the lingual nerve (comes off of mandibular nerve)