MODULE 4: sensory Flashcards
components of afferent nervous system
Somatic pathway
▪ General : “touch”, proprioception (sense of where body parts are)
▪ Special : vision, hearing, balance
Visceral pathway :
▪ General : nociception, physiological receptors (maintian homeostasis)
▪ Special : olfaction, gustation
neurone classes
- afferent neurons
–> sensory neurons provide environmental information to
the CNS
–> convey info to brain - interneurons
- -> integrate information and formulate a response - efferent neurons
- -> carry instructions from the CNS to the effector organs
receptor adaption: tonic vs phasic
sustained stimulation leads to adaptation of the receptor
tonic –> adapt slowly
e.g. vision, touch
phasic –> adapt rapidly
e.g. some pain receptors
lateral inhibition
increases acuity by dampening neighbouring sensory receptors
receptor types (8)
solute –> work on lock and key design
e.g. taste, smell, neurotransmitter receptors
solvent –> work on pressure or turgidity, i.e. a change in membrane
e.g. mechanical receptors
photoreceptors –> respond to photons via opsins
chemoreceptors –> true lock and key mechanism i.e. respond to specific mechanism
mechanoreceptors –> sensitive to mechanical energy
osmoreceptors –> detect change in concentration in bodily fluids
nociceptors –> pain receptors, similar to high threshold mechanoreceptors
thermoreceptor –> sensitive to heat and cold (and capacin/menthol)
structures in the human eye
Cornea
- transparent i.e. no vascularisation as to not impair vision
- immune privilege i.e. no immune response, takes strong infection to cause disruption
- 5 layers for mechanical protection, epithelium is touch sensitive
- barrier to UV
- most of the refractive power
- sensory receptors for reflexes
- fixed focusing power (because cannot change shape)
Lens
- adaptive focusing power
- no vascularisation
- accommodation (contractive power, close focus = muscle relax)
- UV filter
Retina
- receptor layer
- pigment epithelium at base absorbs light so there is no reflection
- this improves acuity and directionality
Fovea
- best focus, allows us to see fine details
- sits inside macula
- 1 photoreceptor / ganglion cell in macula –> no overlap in receptive fields –> discern fine details
Optic Disc
- where nerves exit
- “blind spot”
- vision of other eye compensates
refraction in the human eye
- when light hits boundary between two mediums, light bends
- eye contains mediums with different refractive index
- light changes direction when entering eye
- increases sensitivity of eye i.e. able to focus on different things by changing RI of lens
photoreceptors
inner segment:
- nucleus & mitochondria
outer segment:
- membrane stacking
- in cone, membrane folds
- in rod, free floating discs
IPRGC:
- intrinsically photosensitive retinal ganglion cells
- don’t need photoreceptors to measure amount of light
- contain melanopsin which allows them to complete photo-transduction
- involved in reflex
Rods • 120 millions / retina • High sensitivity • Low acuity • More pigments • Achromatic and night vision
Cones • 6 millions / retina • Low sensitivity • High acuity • Three pigment types • Chromatic vision
adaption to darkness - rods and cones
cones adapt to low light very quickly
cones do not provide effective vision in darkness
rods can adapt to much lower levels of light, but takes longer
colour vision
we can see colour because the eye contains different pigments each with different absorbance
i.e. different peaks of optimal detection
the ratio is what is important wavelengths and intensity confounded because photoreceptor alone cannot direction based on these S -M - L --> green : 0% – 100% – 80% --> blue: 55%–45%–35% --> orange : 0% – 20% – 60%
phototransduction in rods
1) light photon enters eye and hits retina.
2) photons change retinal from cis to trans conformation
3) photon activates transducins
4) transducins release alpha subunit which connects to phosphodiesterases
5) phosphodiesterase turns cyclic GMP to GMP which amplifies signal
6) when cGMP concentration lowers, unselective cation channels close
7) MP in rods hyperpolarises (base state is depolarised, more intense light = more hyperpolarisation)
8) hyperpolarisationg closes VG calcium channel
THESE STEPS ARE DESIGNED TO AMPLIFY SIGNAL
easy to control pathway at each step
retinal circuit
- diagram*
1. photoreceptors hyperpolarise (don’t release neurotransmitters)
- horizontal cells hyperpolarise
- –> connect to bipolar cells via gap junctions
- –> very fast connection - bipolar cells hyperpolarise
- –> connect photoreceptors to ganglion cells
- –> can connect one to one or multiple photoreceptors to one ganglion - ganglion cells produce AP and project to brain
info goes vertically (photoreceptor to ganglion cells)
info also goes horizontally —> detects all features in vision
retina cell types: horizontal cells
horizontal cells sit in between photoreceptors and bipolar cells
connect via gap junctions
cover large area of retina i.e. cover receptive field of large number of photoreceptors
horizontal cells estimate average intensity across many receptive fields
work via lateral inhibition
retina cell types: bipolar cells
connect photoreceptors and ganglion cells
hyperpolarised = off bipolar cell:
convert light energy into inhibition i.e. see light and stop actions potentials
depolarised = on bipolar cell:
see light and have action potential
1-20 photoreceptors connect to 1 bipolar cell
many different sub-types
e. g. midget bipolar cells
- in fovea
- important for high acquity
retina cell types: amacrine cells
connect with bipolar cells and retinal ganglion cell
similar to horizontal cells in organisation, but have many more sub-types (classified by dendrite field)
wise connection range = GABA
narrow connection range = glycine
integrates information horizontally
creates local subunits (bipolar cells + ganglion) that encode one feature e.g. detect motion, detect colour vision, etc
retina cell types: ganglion cells
receive info from bipolar cells and transmit to brain
–> only output of retina
have ON or OFF response
subtypes depending on no. of connections
on/off pairs in ganglion cells: colour vision
- S-cone sends info to ON bipolar cell to activate it
- activates next ganglion cell in line via direct synapse
- amacine cell receives info
- amacrine cell activated and will inhibit retinal ganglion cell
- retinal ganglion cell does not fire
- this inverts signal from cone
- colour observed by ratio of activation
- connect cone from different colour to system i.e. M-cone
- this gives intensity level of light
- weak blue light and strong green light activate S-cone in same way
- connect M-cone to act as light intensity detector
- M-cone acts via off bipolar cell
on/off pairs in ganglion cells: edge enhancement
centre of retinal ganglion cell receives light for large visual field
responds differently to positioning of light (i.e. centre or edge)
either on centre / off exterior or vice versa
on centre + light in centre = more APs
off centre + light in centre = less APs
same for periphery
very important in feature discrimination
- cones connected to horizontal cells
- horizontal cells integrate info from whole receptive field
- light in centre = strong signal in middle which dampens at edges
- bipolar cells & amacrine cells filter signal
- inhibit responses from cones at edges to make ganglion response strong at middle and weak at edges
- —-> LATERAL INHIBITION
two stream hypothesis
hemi-spatial neglect / visual agnosia
two pathways in neural processing of vision: ventral vs dorsal
- -> info either goes to dorsal or ventral part of brain
- -> dorsal = info about where object is i.e. positional features
- -> ventral = info about what object is
- -> allows retina to discern intensity and position of light
- -> signal gets more complex as it travels
hemi-spatial neglect = dorsal pathway disruption
- -> failure of perception, not sensation
- -> patients can see left field but cannot perceive it
visual agnosia = ventral pathway disruption
–> can copy images but do not recognise what they are
–> can be limited to specific category
▪ faces (associative propopagnosia)
▪ words (pure alexia)
▪ colors (color agnosia)
anatomy/function of the ear: outer ear
- outer ear is everything covered by skin
- collect and conduct sound
- amplify the sound waves
- help with direction discrimination
anatomy/function of the ear: middle ear
- connection between sinus and ear
- allows pressure equalisation (prevents breaking tympanic membrane)
- pressure waves of sound pushes on timpanic membrane to move small bones
- stapes connected to oval window —> pushes on scala vestibuli —> filled with non-compressible liquid
- liquid pushes down to round window
- tympanic membrane pulled by round window, which moves malleus again
= SOUND AMPLIFICATION - muscles in ear prevent movement during loud sounds to prevent deafening
anatomy/function of the ear: inner ear
- contains receptors for balance and hearing
- hearing occurs mainly in cochlea –> vibrations sensed by cochlea
anatomy/function of the ear: cochlea
- fluid filled spiral tube
- three scalae (chambers)
- endocochlear potential ([K+] ptential important for sound transduction)
- Organ of Corti, where sound is transduced
- afferent sensory neurons are the SGC (spiral ganglion cells)
anatomy/function of the ear: organ of corti
- transduction occurs through inner hair cells
- —> 1 row of inner hair cells
- —> 3 rows of outer hair cells
- cells perceive motion between basal and tectorial membranes
- membranes not directly connected —> can move independently
- pressure from middle ear pushes basal membrane upwards/downwards
- outer hairs detect this sounds via proteins - contract or elongate to amplify movement
- —> depolarization = shorten
- —> hyperpolarization = lengthen
anatomy/function of the ear: hair cells
- hair cells are mechanoreceptors
- contain ~100 sterocilia each, organised from small to large and connected with tip links
- too loud = motion too strong = serocilia destroyed
- bending towards the largest cilium opens mechanically gated cation channels
- —> transduction channels open
- —> voltage-gated Ca2+ channels open
- —> neurotransmitter vesicles are released
- —> the afferent neurons fire APs
- bending away closes the transduction channels
- —> hyperpolarisation decrease release
- —> silence the afferent neuron
- the stronger the bending, the stronger the signal
features discrimination: pitch vs frequency
frrequency discriminated by place pitch is coded in cochlea
each region of the cochlea is more attuned to a given frequency
envelope maximum = movement of membrane depends on frequency (biggest movement = max)
features discrimination: loudness vs intensity
loudness encoded by intensity of movement
on average, higher frequency perceived as quieter
population coding = membrane moves more = more cells activated
- tensor tympanic muscle stiffens membrane
- stapedius muscle holds stapes in place
- these muscles prevent movement and reduce transduction
coincidence detection
- sound hits left ear first
- signal arrives to right ear later than left ear
- delay line of neurons
- neuron not stimulated until signal from both ears has reached
auditory pathway
- cochlear nucleus filters self-stimuli and preprocess data
- superior olive and trapezoid body fuse binaural information and compute ITD and ILD
- inferior colliculus does some integration (possibly multi-modal)
- MGNT further processes and integrate
- auditory cortex is involved in “perception”, speech recognition
hearing loss
- conductive hearing loss –> lose ability to transduce sound to movement (destroy tympanic membrane)
- sensoryneural hearing loss –> lose ability to transduce pressure to neuronal signals (mutation in K+ channel)
with age, can’t distinguish higher frequency
loud noises can destroy hair cells = cell death
anatomy of the vestibular system
all vestibular receptors found in inner ear
semicircular canals
- 3 orthogonal channels
- ampullae are were the hair cells are located
- sense rotational motion
otoliths
- 2 otoliths
- calcium carbonate crystals
- sense linear acceleration
anatomy of the labyrinth
Saccule and Urticle
▪ Endolymph also high [K+]
▪ Sit on top of hair cells (macula)
▪ Otoconia (bristles) increase density of the otolith
▪ Hair cells are divergent
▪ Polarity is inverted between saccule and
utricle
▪ Saccule is vertical, utricle ~ horizontal
Semicircular canal
▪ Hair cells are bound to the cupula (gel structure)
▪ All share the same orientation
▪ Friction will slowly bring endolymph and
the walls in sync
▪ 3 axis
▪ In rotation, one ear detects rotation and is excited, other side is inhibited
vestibular pathway
labyrinth –> source of sensory output
2nd order neurons in vestibular nuclei —> start processing info by integrating info from both sides of head
- translation only
- roll only
- roll + translation (0g)
- roll + translation (0.4g)
thalamic nuclei integrate info from different senses
efference copy
- copy of motor command needed to filter internal stimuli
- inhibit response from self generated sensory signal –> only external stimulus remains
passive (whole body) rotation activates the neuron
- no efference copy
- pnly vestibular input
active head movement does not activate the neuron
- efference copy available
- theoretical response supressed
both active and passive head movements activate the neuron
