Physiology of Gustation and Olfaction (Pierce) Flashcards

1
Q

loss of sense of smell

A

anosmia

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2
Q

loss of sense of taste

A

aguesia

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3
Q

chemical compounds that bind taste receptors and impart the primary flavor categories (sweet, salty, bitter, sour, unami)

A

tastants

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4
Q

chemical compounds that bind odorant receptors and impart and odor

A

odorants

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5
Q

What is the structure of taste cells?

A
  • taste bud cells are specialized epithelial cells
  • apical domain (location of chemosensory transduction): contains microvilli, tastant receptors, voltage-gated ion channels, and TRP receptors
  • basolateral domain (location of NT release): release of serotonin and ATP
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6
Q

How do tastants elicit an AP?

A
  • ligand (tastant) binds receptor on apical domain
  • receptor potentials of taste cells are usually depolarizing
  • depolarization opens voltage-gated calcium channels and triggers transmitter release
  • NT and mechanism of release differs by cell type
  • NT binding to receptor on nearby primary sensory afferent terminal generates a receptor potential > action potential
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7
Q

What are the associated stimuli and NT’s for each tastant?

A
  • sour: stim is H+ ions (acids), NT is Serotonin
  • salty: stim is Na+ binding ENaC, NT is Serotonin
  • sweet: stim is sugars binding GPCRs, NT is ATP
  • unami: stim is glutamate binding mGluR4 (GPCR), NT is ATP
  • bitter: stim is various compounds binding GPCRs, NT is ATP
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8
Q

How are odorants detected as smell?

A
  • through odorant receptor neurons (ORNs) that are extremely sensitive to odorants
  • olfactory cells are bipolar neurons that release glutamate as their NT
  • ~12 million odors can be detected through ~350 odorant receptors: this diversity of smell occurs b/c one odorant can stimulate more than one type of OR which creates a unique combination or “signature” of that odorant
  • also, conc of odorant matters (e.g. indole smells floral at low conc and putrid at high conc)
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9
Q

How do odorants elicit an AP?

A
  1. odorants diffuse into nasal mucus, bind receptor proteins on olfactory cilia, and activate olfactory cell
  2. olfactory receptor proteins are GPCR’s called Golf receptors
  3. uses second messenger transduction systems (cAMP)
  4. this opens cyclic-nucleotide gated channels (CNGC) allowing Na+ and Ca2+ to influx into cell
  5. depolarization occurs
  6. Ca2+-gated Cl- channels open that provides remainder of depolarization needed to generate appropriate receptor potential to achieve action potential
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10
Q

How do ORN’s adapt to a smell?

A

(when you “get used to” a smell and no longer notice its strength)

  1. receptor potential is reduced in magnitude when cAMP conc drops due to enzymatic break-down
  2. in addition, recovery depends on binding of calcium to calmodulin (Ca2+-CAM) reduces affinity of channel to cAMP, reducing cation influx
  3. odorant receptor itself can become phosphorylated, which modifies its sensitivity to odorants
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11
Q

What is the significance of the high-binding affinity of bitter tastants to their associated receptor?

A
  • bitter taste = innately aversive: thought to guard against consuming poisons, many of which taste bitter to humans
  • as a result, bitter-tuned GPCRs bind their ligand w/ very high binding affinity compared to other taste receptors
  • evolved as a means to detect poisons at very low conc so to avoid additional ingestion of potentially toxic substance
  • people can still learn to tolerate and seek out certain bitter and sour tastants, such as caffeine (bitter), green leafy vegetables (bitter), and citric acid (sour)
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12
Q

What is the physiological significance of tastants?

A
  • sweet: signals presence of carbs that serve as energy source
  • salty: governs intake of Na+ and other salts, essential for maintaining body’s water balance and blood circ
  • umami: believed to reflect a food’s protein content due to presence of glutamate and few other AA’s
  • sour: signals presence of dietary acids, b/c sour is generally aversive, we avoid ingesting excess acids and overloading mechanisms that maintain acid acid-base balance for body; also spoiled foods are often acidic thus are avoided
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13
Q

What are the causes of age related decrease in gustation/olfaction and what consequences do these changes have?

A
  • gustatory: especially after 60, number of taste buds decrease, remaining taste buds shrink in size, mouth prod less saliva
  • olfactory: esp after age 70, decreased nasal mucus prod, fibers and receptors of ORNs decrease
  • exogenous causes: meds, diseases, smoking, pollutants, toxins in air
  • consequences: adults add more salt/spices, can be problematic for older individuals w/ HTN or electrolyte/fluid problems; safe/effective salt sub has yet to be developed; loss of taste/smell results in appetite suppression and may lead to weight loss, malnutrition, impaired immunity, depression, and deterioration of medical conditions
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14
Q

What is the relationship between gustatory/olfactory development in utero?

A
  • sense of smell/taste begin in utero
  • primes growing fetus to taste amniotic fluid which reflects composition of maternal diet
  • maternal diet represents external environment to which fetus would eventually be exposed
  • primes rooting for breastmilk after birth through smell/taste sensitivity (looking for familiar tastes/smells, aka what mom was eating in utero)
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15
Q

How do newborns react to sweet tastants?

A
  • respond in a pattern similar to pleasurable stimulation
  • sweet tastes act as analgesics in infants and children during minor, painful procedures
  • small amnts of sweet solution is placed on tongue of crying newborn to exert a rapid, calming effect along w/ decreased heart rate
  • must be placed in oral cavity b/c direct stomach loading does not result in same outcome
  • sucrose used to reduce procedural pain in infants w/ single painful events (heel lance, venipuncture, circumcision)
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16
Q

What is the mechanism for analgesic effect of sweet-solutions on new borns?

A
  1. general brain arousal suppressed, leading to infant being distracted from procedure
  2. rewarding effect of sweet flavors blunts stress-reponse, promoting calmer affect
  3. anti-nociceptive action: sweet-taste induced beta-endorphin release, activating endogenous opioid system
17
Q

What are thought to be the causes of age-related decline in preference of sweetness?

A
  • preference for sweetness early in life is thought to be linked to child’s need for calories, and nutrient-source would invariably be less important in adulthood
  • although, non-nutritive sweeteners have made it physiologically unreliable to biologically link levels of sweetness w/ caloric intake or energy-content
18
Q

How can the bitter taste of certain meds be masked?

A
  • sodium salts (monosodium glutamate and sodium gluconate) suppress bitter taste at level of the bitter-receptor
  • sugars suppress the sense of bitterness at the cognitive level
  • also, caffeinated and alcoholic beverages often contain added sweeteners, which provide well-liked sweetness and mask unwanted bitterness of caffeine/alcohol
19
Q

What 3 brain regions comprise the “gustatory cortex”?

A
  • postcentral gyrus
  • frontal operculum
  • insula
20
Q

Describe the general gustatory pathway:

A
  • perception of flavor requires somatosensory info from mouth (CN VII ant 2/3 of tongue, CN IX post 1/3 of tongue, and CN X epiglottis), gustatory input from gustatory cortex, and olfactory input from olfactory cortex
  • general pathway: somatosensory info from mouth > nucleus tractus solitarius sends and receives info from hypothalamus and amygdala > NTS projects into to VPM of thalamus > gustatory cortex > orbitofrontal cortex > gustatory cortex also sends info to amygdala
21
Q
  • early site of gustatory-visceral intergration
  • sends info to VPM of thalamus
  • sends/receives info from hypothalamus and amygdala
  • innervation from other branches of vagus relaying info about visceral activity also term here
A

nucleus tractus solitarius (NTS)

22
Q

What are the functions of VPM and gustatory cortex in taste?

A
  • VPM: relay station for taste perception, begins discriminative aspects of taste
  • gustatory cortex: discriminative aspects of taste
23
Q

integrates visual, somatosensory, olfaction, and gustatory stimuli to develop sensation of taste

A

orbitofrontal cortex

24
Q
  • provides affective aspects of eating, emotional context to eating, and memories of eating
  • receives info from gustatory cortex
  • sends/receives info from NTS
A

amygdala

25
Q
  • integrates homeostatic mechanisms of eating (such as hunger)
  • sends/receives info from NTS
A

hypothalamus

26
Q

interplay between eating and calming effects of food involves this system and reward system

A

limbic system

27
Q
  • forms basis for salivating, mimetic responses, and swallowing
  • system within the NTS
A

medullary reflex arcs

28
Q

What is the role of olfactory mucosa in olfaction?

A
  • olfactory neurons/receptors and supporting cells are present in the mucosa
  • one olfactory neuron expresses same odorant receptor on all its cilia
  • the projections of similar odorant receptors are collected into one glomerulus (in the olfactory bulb)
29
Q

What structures and cells are present in the olfactory bulb?

A
  • olfactory glomerulus
  • mitral cells
  • perigolmerular cells
  • granule cells
30
Q

What is the olfaction pathway in terms of the cells comprised in the mucosa and bulb?

A
  • olfactory neurons synapse onto glomeruli and release glutamate (olfactory nerve layer)
  • periglomerular cells are local interneurons and release GABA (increases specificity of signal, glomerular layer)
  • mitral cells and tufted cells project to olfactory tract (external plexiform and mitral cell layers)
  • granular cells are local interneurons and release GABA (increases specificity of signal, granule cell layer)
31
Q

What does the olfactory cortex consist of and where does it project to?

A
  • consists of: anterior olfactory nucleus, olfactory tubercle, piriform cortex, anterior cortical amygdaloid nuclei, periamygdaloid cortex, and lateral entorhinal cortex
  • projects to: intrinsic projections within cortex itself, back to olfactory bulb, thalamus, orbitofrontal cortex, lateral hypothalamus, and hippocampus

(only sensory system that does not route through thalamus before connecting to cortex)

32
Q
  • relay station to ipsi- and contralateral bulb and cortices (olfactory)
  • poorly understood
A

anterior olfactory nucleus

33
Q
  • control of appetite in relation to olfaction
  • olfactory input influences appetite and hunger
A

piriform cortex > lateral hypothalamus

34
Q
  • integration of taste, sight, and smell
  • appreciation of flavor of food
A

piriform cortex > thalamus > medial orbitofrontal cortex

35
Q
  • emotional learning and olfactory fear conditioning
A

anterior cortical amygdaloid nucleus

36
Q
  • integration of emotional aspect elicited by odor
A

periamygdaloid cortex

37
Q
  • important in memory formation in terms of olfaction
  • olfactory input facilitates both memory formation and recall
  • connections within limbic system and this area are responsible for highly evocative experience of memory upon odor sensation
A

entorhinal cortex > hippocampus

38
Q

What are the different causes of altered smell sensations?

A
  • reversible hyposmia: possibly from a head cold that thickens mucosa and blocks odorants
  • head trauma: can shear olfactory bulb from cribiform plate
  • hypersomia: possible in migraines, psychotic stress, and pregnancy

(neurogenesis thought to occur only in 2 places in brain: olfactory bulb and dentate gyrus of hippocampus)

39
Q

What is the relationship between neurodegenerative diseases and smell?

A
  • olfactory impairment is common finding in neurodegenerative diseases
  • Parkinson’s: neurons of olfactory system are among first to demonstrate pathology, even sometimes years before motor deficit is manifested
  • olfactory testing can be used as a biomarker for early diagnostic strategies and prediction of clinical outcomes due to neurodegenerative diseases