Lecture 1 The chemical senses
The ability to taste (gustation) and smell (olfaction).
Life evolved in the sea. With their villi, they could move towards e.g. nutrient sources and move away from toxins.
Chemoreceptors: chemically sensitive cells
➢ G-protein coupled receptor (GPCR): 7 alpha helices that span the membrane.
Activation of receptor → activation/inhibition of G protein → activation/inhibition of an intracellular signal
cascade.
Chemoreceptors:
➢ Taste and smell: detection of ‘’environmental chemicals’’
➢ Discrimination between new nutrient sources and potential toxins.
➢ Important for survival!
➔ Mouth and nose are ‘’gatekeepers’’ of the internal milieu.
Internal (chemo)sensory information:
➢ Gastrointestinal system
➢ CO2 and O2 detection in circulation
➢ Muscle (lactic acid accumulation)
➢ Each cell has the ability to detect chemical substance, for detection of internal stressors → physiological
boundaries of homeostatic barriers.
Wilder Penfield: mapping of primary somatosensory cortex.
He applied electric currents to the surface of brains of epileptic patients. Since the patients were awake during the
operations, they could tell Penfield what they were experiencing. Probing some areas triggered smell, taste, and
sometimes whole memory sequences.
Sensory Homunculus:
➢ 40% of all sensation from the mouth and face.
➢ Intestines about 5% of sensation.
The brain is NOT static, so the brain of an adult IS changing.
If you use a part of your body a lot, the representation of that part on the somatosensory cortex increases.
➢ ‘’Details of cortical map structure are largely created and altered by experience’’
,Taste and smell:
➢ Have connections to internal drives:
- Hunger
- Thirst
- Emotion
- Sex
- Memory
➢ Taste and smell serve this input in different ways
➢ Taste and smell (and with texture of the food) work together: → ‘’flavour’’
Basic tastes:
➢ Sweetness: fructose, sucrose, aspartame, saccharin.
➢ Saltiness: NaCl
➢ Sourness: acid H+
➢ Bitterness: K+, Mg2+, quinine, complex organics.
➢ Umami, MSG (monosodium glutamate): meaning ‘’yummy’’ in Japanese. MSG doesn’t have a taste itself, but
it can increase the tastiness of the other 4 basic tastes.
What is a flavour? How can we dissociate those?
Food is (often) a combination of taste + smell + other sensory modalities (texture, temperature, visual
characteristics).
This doesn’t mean that localisation is specific for that taste.
→
Also palate (= gehemelte), pharynx (= keelholte)
and larynx(= strotklep) contribute to taste
sensation.
Papilles: the taste-sensitive structures.
➢ Vallate papillae: the largest and most posterior papilles.
➢ Foliate papillae: are elongated.
➢ Fungiform papillae: are relatively large toward the back of the tongue
and much smaller along the side and tip.
Taste bud: cluster (50-100) of taste cells extended into the taste pore, the site where chemicals dissolved in saliva
can interact directly with taste cells.
,Supertasters: have higher numbers of taste buds. Foods in general are too intense for these folks. Beware of these
people in taste panels, because they are not average tasters.
Taste receptor cells:
➢ 90% of receptor cells react to 2 tastants or more.
➢ Just above threshold taste receptor cells are sensitive to one tastant.
Cell 1:
➢ NaCl: membrane depolarisation
➢ Quinine, HCl, and sucrose: hyperpolarisation
Cell 2:
➢ NaCl, quinine, and HCl: membrane depolarisation
➢ Sucrose: hyperpolarisation
➔ Activation of gustatory afferent axon upon membrane
depolarisation
Different responses of action potentials (= different tastes)
has different transduction mechanisms:
Taste transduction:
1. Passage of ions through channels (saltiness and sourness).
2. Binding (or blockade) of ion-channels (sourness).
3. Binding to G-protein coupled receptors (sweetness, bitterness)
1 + 2. Saltiness and sourness:
Interaction of tastants with ion channels:
- By passage (Na+ and H+)
- By blockade (H+ blocking K+ channels).
Causes membrane depolarization, Ca2+ influx, and
transmitter release.
Saltiness:
Na+ enters taste cell through channel → membrane
depolarization → opening of other ion channels → Na+
and Ca2+ can flow into the cell → opening of synaptic
vesicles → release of neurotransmitter into synaptic
cleft → stimulates gustatory afferent axon
Sour:
H+ enters taste cell through channel → blockade of K+
channel → membrane depolarization → Na+ and Ca2+
can flow into the cell → opening of synaptic vesicles →
release of neurotransmitter into synaptic cleft →
stimulates gustatory afferent axon
, 3. Sweetness and bitterness:
T1 receptors (T1R) and T2R: GPCRs activate:
- Phospholipase
- Inositol triphosphate (IP3)
- Ca2+ release
→ Leading to transmitter release.
T1R: minimally 3 types (T1R1, T1R2, T1R3)
T2R: 30 different ones for bitterness. Each taste receptor cell expresses all (probably),
but in different quantities.
T1R and T2R are connected to a G-protein → activation of G-protein → formation of
IP3 → causes opening of Ca2+ stores inside the cell + membrane polarization → influx
of Ca2+ and Na+ → vesicles fuse with the membrane → release of neurotransmitter →
activates gustatory afferent axon.
Different taste bud cell types:
➢ Type I glial-like cell: involved in salty tasting.
➢ Type II receptor cell: involved in sweet, bitter, and umami tasting.
➢ Type III presynaptic cell: involved in sour tasting.
Phenylthiocarbamide: bitter taste
People react very differently to bitter taste.
This is caused by mutations in TAS2R38 gene.
Besides the 5 basic tastes, there’s also an indication that fat can be tasted.
This occurs through the CD36 receptor.
CD36 (Cluster of Differentiation 36):
➢ Member of class B scavenger receptors.
➢ Binds collagen, thrombospondin, erythrocytes, LDL, phospholipids, and
long-chain fatty acids.
➢ Is involved in fatty acid and glucose metabolism, dietary fat processing.
➢ Errors may cause atherosclerosis, hypertension, diabetes,
cardiomyopathy, and Alzheimer’s disease.
SNP in CD36 gene → higher sensation of increased creaminess → preference for high fat foods → risk towards
obesity.
The ability to taste (gustation) and smell (olfaction).
Life evolved in the sea. With their villi, they could move towards e.g. nutrient sources and move away from toxins.
Chemoreceptors: chemically sensitive cells
➢ G-protein coupled receptor (GPCR): 7 alpha helices that span the membrane.
Activation of receptor → activation/inhibition of G protein → activation/inhibition of an intracellular signal
cascade.
Chemoreceptors:
➢ Taste and smell: detection of ‘’environmental chemicals’’
➢ Discrimination between new nutrient sources and potential toxins.
➢ Important for survival!
➔ Mouth and nose are ‘’gatekeepers’’ of the internal milieu.
Internal (chemo)sensory information:
➢ Gastrointestinal system
➢ CO2 and O2 detection in circulation
➢ Muscle (lactic acid accumulation)
➢ Each cell has the ability to detect chemical substance, for detection of internal stressors → physiological
boundaries of homeostatic barriers.
Wilder Penfield: mapping of primary somatosensory cortex.
He applied electric currents to the surface of brains of epileptic patients. Since the patients were awake during the
operations, they could tell Penfield what they were experiencing. Probing some areas triggered smell, taste, and
sometimes whole memory sequences.
Sensory Homunculus:
➢ 40% of all sensation from the mouth and face.
➢ Intestines about 5% of sensation.
The brain is NOT static, so the brain of an adult IS changing.
If you use a part of your body a lot, the representation of that part on the somatosensory cortex increases.
➢ ‘’Details of cortical map structure are largely created and altered by experience’’
,Taste and smell:
➢ Have connections to internal drives:
- Hunger
- Thirst
- Emotion
- Sex
- Memory
➢ Taste and smell serve this input in different ways
➢ Taste and smell (and with texture of the food) work together: → ‘’flavour’’
Basic tastes:
➢ Sweetness: fructose, sucrose, aspartame, saccharin.
➢ Saltiness: NaCl
➢ Sourness: acid H+
➢ Bitterness: K+, Mg2+, quinine, complex organics.
➢ Umami, MSG (monosodium glutamate): meaning ‘’yummy’’ in Japanese. MSG doesn’t have a taste itself, but
it can increase the tastiness of the other 4 basic tastes.
What is a flavour? How can we dissociate those?
Food is (often) a combination of taste + smell + other sensory modalities (texture, temperature, visual
characteristics).
This doesn’t mean that localisation is specific for that taste.
→
Also palate (= gehemelte), pharynx (= keelholte)
and larynx(= strotklep) contribute to taste
sensation.
Papilles: the taste-sensitive structures.
➢ Vallate papillae: the largest and most posterior papilles.
➢ Foliate papillae: are elongated.
➢ Fungiform papillae: are relatively large toward the back of the tongue
and much smaller along the side and tip.
Taste bud: cluster (50-100) of taste cells extended into the taste pore, the site where chemicals dissolved in saliva
can interact directly with taste cells.
,Supertasters: have higher numbers of taste buds. Foods in general are too intense for these folks. Beware of these
people in taste panels, because they are not average tasters.
Taste receptor cells:
➢ 90% of receptor cells react to 2 tastants or more.
➢ Just above threshold taste receptor cells are sensitive to one tastant.
Cell 1:
➢ NaCl: membrane depolarisation
➢ Quinine, HCl, and sucrose: hyperpolarisation
Cell 2:
➢ NaCl, quinine, and HCl: membrane depolarisation
➢ Sucrose: hyperpolarisation
➔ Activation of gustatory afferent axon upon membrane
depolarisation
Different responses of action potentials (= different tastes)
has different transduction mechanisms:
Taste transduction:
1. Passage of ions through channels (saltiness and sourness).
2. Binding (or blockade) of ion-channels (sourness).
3. Binding to G-protein coupled receptors (sweetness, bitterness)
1 + 2. Saltiness and sourness:
Interaction of tastants with ion channels:
- By passage (Na+ and H+)
- By blockade (H+ blocking K+ channels).
Causes membrane depolarization, Ca2+ influx, and
transmitter release.
Saltiness:
Na+ enters taste cell through channel → membrane
depolarization → opening of other ion channels → Na+
and Ca2+ can flow into the cell → opening of synaptic
vesicles → release of neurotransmitter into synaptic
cleft → stimulates gustatory afferent axon
Sour:
H+ enters taste cell through channel → blockade of K+
channel → membrane depolarization → Na+ and Ca2+
can flow into the cell → opening of synaptic vesicles →
release of neurotransmitter into synaptic cleft →
stimulates gustatory afferent axon
, 3. Sweetness and bitterness:
T1 receptors (T1R) and T2R: GPCRs activate:
- Phospholipase
- Inositol triphosphate (IP3)
- Ca2+ release
→ Leading to transmitter release.
T1R: minimally 3 types (T1R1, T1R2, T1R3)
T2R: 30 different ones for bitterness. Each taste receptor cell expresses all (probably),
but in different quantities.
T1R and T2R are connected to a G-protein → activation of G-protein → formation of
IP3 → causes opening of Ca2+ stores inside the cell + membrane polarization → influx
of Ca2+ and Na+ → vesicles fuse with the membrane → release of neurotransmitter →
activates gustatory afferent axon.
Different taste bud cell types:
➢ Type I glial-like cell: involved in salty tasting.
➢ Type II receptor cell: involved in sweet, bitter, and umami tasting.
➢ Type III presynaptic cell: involved in sour tasting.
Phenylthiocarbamide: bitter taste
People react very differently to bitter taste.
This is caused by mutations in TAS2R38 gene.
Besides the 5 basic tastes, there’s also an indication that fat can be tasted.
This occurs through the CD36 receptor.
CD36 (Cluster of Differentiation 36):
➢ Member of class B scavenger receptors.
➢ Binds collagen, thrombospondin, erythrocytes, LDL, phospholipids, and
long-chain fatty acids.
➢ Is involved in fatty acid and glucose metabolism, dietary fat processing.
➢ Errors may cause atherosclerosis, hypertension, diabetes,
cardiomyopathy, and Alzheimer’s disease.
SNP in CD36 gene → higher sensation of increased creaminess → preference for high fat foods → risk towards
obesity.
