Lecture 24 - Taste Flashcards
Gustation
taste
Olfaction
smell
What is the stimulus?
The sensations of taste and smell arise in response to contact with chemicals in the environment, either that we put in our mouth (tastes), or that we inhale (odours)
The cells that detect these stimuli, therefore, are chemoreceptors (sensors able to detect chemicals)
What do the chemical senses do?
Allow us to detect chemicals in the environment that might help us survive and fulfill our biological destiny!
Information of taste and smell goes to very primitive part of the brain which triggers emotional responses and behaviours
Finding food and avoiding poisons
Finding a compatible mate (once sexual maturity has been reached)
taste buds in
tongue papillae
taste buds in the tongue papillae
Bumps and within these papillae are things called taste pores and taste buds are within the taste pores
Present food to a variety of chemoreceptors in our mouth to determine in the first instance whether it is something we should spit out
Natural instinct is that bitter things could be posionous so usually spit it out
Folds of epithelium that lines the sides of our tongue are called the foliate papillae
Even further back there are larger bumps - vallate papillae
Taste pores
Little holes around the outside of papillae
Coming out of these pores are little hairs called microvilli which assess the environment in your mouths at that time
Also in these pores are taste buds which are where our chemoreceptors are located
Taste bud
Also have taste bids on palate (roof of mouth) , pharynx (back of throat) and epiglottis
Taste pores
Little holes around the outside of papillae
Coming out of these pores are little hairs called microvilli which assess the environment in your mouths at that time
Also in these pores are taste buds which are where our chemoreceptors are located
Humans can detect how many different tastes
5
Different tastes
Sweet Sour Salty Umami Bitter
Sweet
Sweet – stimulated by sugars
e.g. fructose
Also stimulated by artificial sugars
Sour
Sour – stimulated by acids
e.g. acetic acids
Salty
Salty – stimulated by sodium (NaCl)
Bitter
Bitter – complex, but typically stimulated by alkaloids
Learnt to regard them as palatable rather than regard them as dangerous, habituation
Umami
Umami – stimulated by amino acids, especially glutamate
E,g, MSG - glutamate stimulates our umami receptors
Taste buds
2000-5000 taste buds, on tongue, palate, pharynx and epiglottis
Each taste bud is a compact cluster of 50/100 columnar epithelial cells (type I, type II and type III)
Different signalling transduction pathways for different tastes
Type II and II are involved in the sensation of taste
Type I cells act more like glial cells rather than being involved in the sensation of taste, more involved in maintenance of homeostasis for the whole taste bud
Type II and III taste bud cells
Type II and II are involved in the sensation of taste
Type I taste bud cells
Type I cells act more like glial cells rather than being involved in the sensation of taste, more involved in maintenance of homeostasis for the whole taste bud
General cell signal transduction mechanism
- Interaction of tastant with receptor causes increase in intracellular Ca2+
- Ca2+ flux causes release of neurotransmitter or signaling molecule which interacts with afferent nerve fibre
- ATP, GABA, serotonin and Ach are transmitters/ signaling molecules involved in taste signaling in taste buds (taste sense is different with lots of different taste molecules)
G-protein mediated signalling in Type II taste cells =
Sweet
Bitter
Umami
G-protein mediated signalling in Type II taste cells - Sweet
Homodimer (2 exact isoforms) of the type I receptor
G-protein mediated signalling in Type II taste cells - Bitter
Monomer of the type II receptor
G-protein mediated signalling in Type II taste cells - Umami
Heterodimer (2 different isoforms) of the type I receptor
Shared steps of G-protein mediated signalling in Type II taste cells for sweet, bitter and umami
Activation of G-protein coupled receptor –> Activation of Phospholipase C
And activity of phospholipase C creates an increase in IP3 and IP3 itself binds to its receptor called IP3R3 which sits in the membrane of the endoplasmic reticulum and when it binds it causes the IP3R3 channel to open and calcium is released from the ER into the cytoplasm
Opening of IP3R3 channel and calcium efflux into cytoplasm
Increase of calcium in the cytoplasm and this causes the opening of the channel TRPM5 which causes a sodium influx which causes a change in membrane potential leading to depolarisation
Opening of TRPM5 channel -> sodium influx -> taste cell depolarisation
Opening of CALHM1 channel -> ATP release -> depolarisation of afferent nerve fibres
Depolarisaiton causes the opening of CALHM1 channel
When this channel is opened the cell releases ATP which then binds to receptor on afferent nerve fibres creating an action potential to be sent off to the brain
Non G-protein signalling in Type III taste cells =
Sour and salty
Steps of Non G-protein signalling in Type III taste cells for sour taste
Stimulated by acids (such as acetic acid or citric acid)
Protons enter the cell via a proton-selective channel (Otop1)
blocks leaky K+ channels
Cell depolarises resulting in the release of neurotransmitter onto terminal of afferent nerve fibre
Under normal conditions, Type III taste cells have a leaky potassium channel which allows potassium out of the cell and maintains membrane potential but when these taste cells are exposed to an acid, protons can enter cell through Otop1 which reduces intracellular pH (makes more acidic) and this reduction in pH blocks the leaky potassium channels so potassium can no longer leave the taste cell which leads to depolarisation of the taste cell which allows sodium to come in and causes an action potential and the action potential causes calcium channels to open and cause calcium influx and get neurotransmitter release onto afferent nerve fibres
Non G-protein signaling in Type III taste cells: Salt (pretty debated)
NaCl, and Na+ containing compounds
Probably sensed by type III taste cells
Na+ likely enters through ENaC (epithelial Na+ channel)
Into the type III taste cell and causes a depolarisation of the cell and depolarisation causes opening of voltage gated calcium channels and cause influx and the increase in calcium results in the release of vesicles containing neurotransmitter to be released onto the afferent nerve fibres
Depolarisation results in release of neurotransmitter onto afferent nerve fibres
Central signal transduction pathway
Taste buds innervated by chorda tympani, lingual, trigeminal and glossopharyngeal nerves
Afferent fibres synapse in the medulla and then…info…
Info relayed to the thalamus, then to the cortex
Motor nerve supply to tongue muscles mainly Hypoglossal (allows tongue movement)
Other ‘tastes’
Spicy foods Peppery (pungent) foods Fatty foods Astringent foods Spiciness and pungency do not interact with specific taste receptors and are therefore not thought of as tastes
Spicy
Hot and spicy “tastes” are sensed by heat and pain-sensitive nerve fibres stimulated by chemicals such as capsaicin and piperine
Capsaicin is an active component of chilli peppers
Piperine is the alkaloid that gives pepper its pungency
Astringent foods
Astringent foods
High amount of tannins
Popcorn, unripened bananas, pomegranates
Causes mucus layers in mouth to contract, leaving your mouth dry
Fatty foods
Fatty foods
Fats believed to interact with CD36 which then activates phospholipase C …cause IP3 increase…IP3 binds to IP3R3 and causes calcium influx…then signal sent to afferent nerve fibres (NOT going to be heavily tested, still debate)
Perception of taste
Our perception of taste is stimulated by the activation of a combination of these receptors
Perception of taste is also heavily linked by smell
The loss of taste caused by …
Neurological damage
Stroke
Smoking
Change in form, quantity and vascularization of taste buds
Infection
e.g. COVID 19
Aguesia
Aguesia (the total loss of taste)
Dysguesia
Dysguesia (persistent horrible taste in mouth)
Hyperguesia
Hyperguesia heightened taste (ABNORMAL)
What depolarises type III taste cells
A reduction in intracellular pH
When are leaky K+ channels blocked?
When pH reduces
Type I cells and taste
not involved in the sensation of taste
Glutamate
Glutamate forms a major part of the umami taste response (also other ones, but this is the major one)
CALHM1
ATP
Otop1
H+/protons into type III taste cells
IP3R3
calcium out of ER cells
Taste transduction in type II taste cells vs type III taste cells
taste transduction in type II taste cells is G protein mediated but in type III taste cells it is not
Angular acceleration =
canals
Linear acceleration
utricle and saccule
Ossicles function
Transmitting sound waves from outer to inner ear = ossicles
