Lecture 7- Special sensory transduction mechanism Flashcards
What is a characteristic of special senses?
• Senses operating at a distance from the information source
What are the special senses?
• Vision • Hearing/audition • Smell/olfaction – Taste/gustation (not technically a special sense, but grouped with the other chemical senses here) – Smell and taste together give flavour (-taste gustation= grouped from other senses= flavour consists of many senses -chilli= noxious normally)
What are some characteristics of vision?
• Light detected in retina at the back of the eye • All vertebrate retinas have same basic layered structure • Light passes through all layers to reach the photoreceptors, except in fovea (primates) • Two broad types of photoreceptors – Rods (low light) and cones (bright light)
How does vision work?
- mechanosensory= depolar -visual= hyperpolarisation so there is more processing
- listen to this again
- albinism= no melanin, that melanin is essential for the function of the eye, if it is not there get back reflection in the eye
- fovea= center of all the visual acuity
- all other layers= so the layers are pushed away so the light comes in to the fovea directly= so you can read properly etc.
- two classes rods= the purple one, rhodopsin in the outer rod then cytoplasmic region (processing) nucleus and axon (really short) any change in the body is there, then terminals -cones= shorter, the outer segment a bit different, coneopsin pigment,
- rods= rhodopsin responds to low levels of light and saturates at higher levels (when it is darker)
- cones= do not saturate as easily but do not respond at low light conditions= so in normal light these are the ones functioning
What happens to photoreceptors when they are hit by light?
- rods are so sensitive that they will detect individual photon of light
- cones wouldn’t
What is the mechanism of vision?
- works the same way for rods and cones, same for most animals
- at rest (in complete dark) the outer segment will have high conc of cGMP (rpoducing that all the time) this activates the cyclic nucleotide deopendt channels that allow calcium to go through= in the dark they will be depolarised (open sodium and calcium channels)
- light on outer segment= will activate chemical reaction= on rhodopsin/coneopsin= then rapid actovation via G protein by phosphodiestarease and breaks down cGMP and by breaking it down= it closes the cyclic nucleotide dependnt channel= reduced sodium flux and hyperpolarisation occurs
How does vision work (2)?
- Light/opsin interaction activates phosphodiesterase to breakdown cGMP
- Low cGMP closes cGMP- dependent Na+ channels
- Closing Na+ channels hyperpolarizes membrane
- Same process in rods and cones, but opsins differ
- Despite being 2nd messenger driven, process is very fast
How is the signal sent from rods/cones to the brain?
- Response in rod prolonged compared with cone
- Many rods converge on one bipolar cell, low light specialization, low acuity
- In highest acuity part of retina (fovea), each cone connects to 1 or 2 bipolar cells
- Note, there are specific rod and cone bipolar cells
- how does hyperpolarising signal in the photorecpetor end up being a change in the AP end up in the brain:
- signal from the eye to the occipital cortex,multiple layers in the eye= photoreceptor layer, bipolar layer, amacrine and ganglion cells, it is the ganglion cells that produce the AP to the brain
- must get from the photoreceptors to the ganglion cells very short axons in teh system so from photp to ganglion do not need AP,
- in fovea= no rods, or very few, that is why you cannot read in low light conditions -in the peripheral vision= mostly rods, larege amount of convergence= low acuity
How does photoreceptor depolarisation influence bipolar cells?
• Photoreceptor terminals continuously release glutamate in the dark • Hyperpolarization at the level of the outer segment leads to hyperpolarization at the terminals of the photoreceptor cells – passive conduction • Hyperpolarization of the terminals leads to reduced influx of calcium ions • Reduced calcium influx leads to reduced glutamate release -from photo to bipolar cells, unlike most cells photoreceptors= they are continously releasing neurotransmitter even when they are not being stimulated (glutamate), special structures to do this -passive conduction through axon onto the dendrites of the bipolar cells= then reduced glutamate release -light= less glutamate released
What must happen to a signal to be perceived by the brain? (vision)
- Glutamate depolarizes some bipolar cells (Off-centre) – Reduced glutamate release from photoreceptors causes off-centre bipolars to hyperpolarize
- Glutamate hyperpolarizes other bipolar cells (On-centre) – Reduced glutamate release from photoreceptors causes on-centre bipolars to depolarize
- Membrane potential change in bipolar dendrite causes similar change in terminals on ganglion cells – passive conduction
- the bipoalr can be divided into two classes depending on how they respond to glutamate
- the off center= depolarised by glutamate, sustained in this state, when light falls onto the input field= get reduction in glutamate= reduction in MP of that cell= so they will hyperpolarise themselves= by turning off glutamate
- on centre cells= hyperpolarised by glutamate= as you the receptive field= the region where the bipolar cells will respond to
- off centre= if light in the centre will switch it on, if peripheral= off
- due to horizontal cells go horizonatlly= synaptic connection with photo and bipoalr and reverse the signal if the light is coming from surround and not the centre -hyper on the surround of the field= the on centre cell
- every neuron has a receptive field= in the eye= region of the retina where the neuron will be activated
- Ganglion cells - only neurons in retina with axons that leave the eye
- Ganglion cells - only retinal neurons that fire action potentials
- Ganglion cells are depolarized by glutamate
- All bipolar cells release glutamate continuously in the dark
- Membrane potential of ganglion cells follows that of input bipolar cells
- the bipoalr cells have the signal, then pass their signal via releasing glutamate onto ganglion cells, the ouput cells in the retina (teh outermost cells, not photosensitive)
- only neuron to fire AP, the projection cells= optic nerve= axons of the ganglion cells, they are depolarised by glutamate
- the ganglion will follow what the bipolar does, on center bipolar connect to on center ganglion
- off centre bipolar will connect to off centre ganglion cells
- also in the LGN (synaptic input of the optic nerve) and then into V1
- light falling on will excite one pathway, and depress another, this is due to the reason that it is easy to tune so can detect small differences
- absence of a signal if a signal is expected is information
- the visual system is continously balancing the presence or absence of a signal
How does olfactory transduction work?
- olfactory sense in humans is relatively rudimentary: -the detection of volatile chemicals, that enter the olfactory region (nose) dissolve in layer of mucous that lines the olfactory epithelium and dtetcted by teh olfactory neurons -few classes of neurons that for sure turn over, stem cells in the olfactory epithelium
- send their axons thriugh cribiform plate into the olfactory bulb
- continuosly turnover of olfactroy neurons that are dying and being replaced by axons from new cells, send olfactory know into the mucous, dissolve into mucous will interact with the cilia and there you get a receptor potential
- about 2000 odourants a human can detec
- the membrane current= depolarisng= down in here, the left green pic. when oddourant falls onto cilia, it will cause an inward current (only if the right receptor) get much smaller current if on the body, so cillia teh crucial bit = depoalrisation!
- individual olfactro yneurons only have receptors for a small number of odourants= that is the only way you can discrimnate
- the receptive field is the odourant the neuron responds to
- scent of cancer= dogs?! -
What is the basic olfactory transduction process?
- Up to 2000 different olfactory receptor proteins
- Each has its own preferred odorants
- All activate Golf to activate adenylate cyclase
- Cyclic AMP activates cAMP dependent cation channel to depolarize membrane and produce a receptor potential
- odourants= what we as humans can smell and describe, then there are more smell activating molecules known as feromones, humans not great at detection
- vomeluronasal organ in some animals= another receptors in there for feromones -recpetor protein in the membrane of teh cilia, each neuron makes its own suite of proetins (1 or 2 usually) have a receptor and when odournat binds= activates G protein (Golf) dissociates into alpha subunit diffuses along to adenylate cylcae that is boun to membrane then will release of ATP to cyclic AMP then diffuse across to cyclic nulceotide gated cation channel (different to vision as here cAMP depenndent) then cahnnel opens and increase in cAMP (opposite direction to the vision)
- activation= influx of Na and Ca throught the nucleotide gated cyclic channel= activate Cl channel= leads to leaving of teh Cl from the cell= and Cl going out is teh equivalent of Na and Ca going in so get depoalrisation = then reorganised by calcium cl exchanegerr= sets it up to resting memnraner potentila
What is the specifity of olfactory receptor neurons?
• Individual neurons respond to more than one odorant • Identification of odorants depends on convergence within pathway • Individual neurons in olfactory bulb only receive input from receptor neurons preferring a single odorant • Processing involves identity of each olfactory neuron responding -olfactory= very specific in the olfactory bulb! -the first ones not as specific,
PIC11How does taste work?
• 5 basic tastes (with one new one) – Salt,sweet,acid,bitter, umami
– Fattyacidrecentlydiscovered
- Salt and acid detected via passage through ion channels in taste cell membrane leading to depolarization
- Sweet, bitter and umami have specific G-protein coupled receptors leading to membrane depolarization
- Depolarization leads to transmitter (glutamate) on to primary afferent terminals
- taste receptors in the mouth and tongue
- umami =monosodium glutamate -differentially located on the tongue
- the umami enhances the flavour of food
- another taste receptors= fatty acids receptors detect fat in your mouth= create the filling feeling
- cannot taste properly unless you have some fat -the mechanism= various depending on teh taste
- the taste recptor cells= like the hair cell= not a neuron! but ativated by chemical recptors in the and leads to release to neurotransmitter to primary afferent neuron
What do you need to know?
• Photoreceptors are hyperpolarized by light – Rods operate in low light, cones in bright light • Photoreceptors use activation of phosphodiesterase by a G- protein (transducin) to reduce cyclic GMP concentration, thereby closing cGMP-dependent Na channels • Photoreceptors release glutamate in dark, light reduces glutamate release • Responses to glutamate determine pathway coding • Chemical senses mediated by a large number of different receptors in membrane of sensory cells that communicate with other neurons via synaptic transmission
