Sensory Physiology Flashcards
afferent division
All input, going in
afferent divides into
- somatic sensory
- visceral sensory
- special sensory
Somatic sensory
general senses:
- touch, pressure, temperature
- external environment
visceral sensory
[glucose], osmolarity, O2, blood pressure
- internal environment
special sensory
- taste, smell, vision, hearing, equilibrium
- external environment (special)
- –> limited to cranial nerves
sensory receptors function
convert chemical/physical stimulus into nerve signal
sensation
awareness of stimulus signal must reach CNS –> cerebral cortex
sensory receptors
- specialized dendritic endings that detect stimulus on neuron
OR - receptor cell that talks to neuron
sense organ
neurons and other tissue that enhance sensory response
ex: eye, ear
thermoreceptors
temperature = warm or cold
photoreceptors
photons of light
- detect light
- produce graded potentials
nociceptors
pain (specialized chemoreceptors)
chemoreceptors
chemicals = NTs, sugars, ions, amino acids. etc.
mechanorecptors
physical deformation (stretch, pressure, touch)
proprioceptors
body position and movement (muscles, tendons, joints)
- specialized mechanoreceptors
receptor potential
stimulus opens ion channels on sensory neuron or sensory cell, which produces a graded potential
- analogous to local potentials
- same characteristics
- most EPSPs
- increase magnitude of stimulus = increase frequency of APs
sensory coding
- intensity
- location
- duration
- type (modality)
receptive field
area that leads to activation of a particular neuron
stimulus intensity
determined by action potential frequency
stronger stimuli can also affect a larger area, which recruits additional afferent neurons –> send more signals
- increase summation of receptor potentials
- stronger stimulus = more ion channels
- open in neuron = more APs
Weber-Fechner Principle
the greater the background stimulus, the greater an additional change must be for it to be detected
- ex: holding 30g weight can barely detect 1g change
- holding 300g weight can barely detect 10g change
- holding 30g weight would notice 10g change
stimulus location
- precision with which we can locate a stimulus is determined by size and overlap of the receptive fields of afferent neurons
- smaller receptive field = more precise indication of location
- receptor density is greatest at center of the receptive field
- visceral organs have large receptive fields = hard to pinpoint stimulus
one large receptive field
stimulus anywhere in receptive field activates same neuron
- back = about 7 cm –> cannot sense 2 touches <7 cm apart
three small receptive fields
finger = about 1 mm –> can sense 2 touches > 1 mm apart
high frequency of APs mean two things
- moderate stimulus at A
OR - strong stimulus at B
lateral inhibition
enhances the contrast between the center and periphery of a stimulated region to pinpoint location
what is the most important mechanism for to pinpoint a location?
lateral inhibition
inhibitory
decreases the number of APs from surrounding neurons
afferent neurons
- recruit inhibitory interneurons to decrease stimulus in adjacent neurons
- greatest inhibition will come from most stimulated neuron
examples of lateral inhibition
- pressing tip of pencil against finger
- hair movement
- retinal processing to increase visual acuity
- temp and pain pathways have poor lateral inhibition (difficult to pinpoint)
sensory adaptation
- despite continued stimulus, AP frequency decrease over time
- become less aware of stimulus
phasic
rapid adaptation
phasic example
smell, hair movement (clothes on skin, hot bath)
tonic
slow adaptation
tonic example
proprioceptors, pain
- must be aware of body position at all times
stimulus type
different receptors have different designs, which make them preferentially sensitive to one stimulus modality
labeled line code
action potentials from each receptor then travel along unique pathways to a specific region of the CNS associated with that modality
ex: will “see” light if pressure on eyeball
sensory pathway
spinal cord –> thalamus –> cerebral cortex
decussate
cross L/R
auditory cortex
temporal lobe
somatosensory cortex
general senses to parietal lobe
taste cortex
parietal lobe
visual cortex
occipital lobe
olfactory cortex
info does NOT go thru thalamus first
- temporal lobe
sensory interpretation
association areas of the cortex integrate and process sensory input into perception
factors that affect perception
- receptor adaptation
- emotions, personality, experience
- filtering by the thalamus
- damaged pathways (ex: phantom limb), drugs
- remember weber-fechner principle
taste
- gustation
- chemoreceptors
where are taste buds found?
lingual papillae
how many taste buds in the mouth and throat
3,000-10,000
vallate papillae
about 250 taste buds each
fungiform papillae
about 3-5 taste buds each
filiform papillae
- sense texture
- mechanoreceptor
primary taste senstations
- sweet
- sour
- salty
- bitter
- umami
sweet
sugars
sour
acids
salty
Na+/K+
bitter
alkaloids
umami
amino acids
physiology of taste
- dissolved food molecule
- chemoreceptor activated on taste cell
- NT released onto sensory neuron
- CNs VII, IX, X take info thru thalamus to gustatory cortex (parietal lobe)
- rapid adaptation
basal cell
stem cells replace taste cells every 7-10 days
perception of taste influenced by:
- differential activation of 5 receptor types
- smell (80%)
- sight
- texture
- temperature
- other substances in foods (ex: that stimulate pain)
- -> ex: spices, peppers
physiology of smell
- odorant molecule dissolved in mucus of olfactory epithelium
- odorant receptor on olfactory cell (neuron) activated (1 of 1000 types)
- labeled line thru olfactory bulb
- rapid adaptation (phasic receptors)
perception of smell influenced by:
- attentiveness
- hunger
- gender
- age
- experience
cochlea
hearing
vestibular branch
equilibrium
sound waves
audible vibration of molecules
frequency
pitch
- cycles of movement per second
- determined by region of basilar membrane displaced = pitch
amplitude
loudness
- magnitude of movement of basilar membrane = increased number of APs
physiology of hearing
- tympanic membrane deflects, “vibrates”
- middle ear bones move
- membrane in oval window moves
- basilar membrane moves by sound vibrations
- tectorial membrane doesn’t move –> hair cells pushed against tectorial membrane
- sterocilia bend against tectorial membrane tip links pull ion channels open (K+)
- K+ flows in to depolarize cell
- Voltage gated Ca+2 channels open
- NT released onto CN VIII (cochlear nerve)
three fluid-filled chambers in the ear
- scala vestibuli
- cochlear duct
- scala tympani
what contains endolymph?
cochlear duct
what contains perilymph
- scala vestibuli
- scala tympani
perilymph
similar to CSF
endolymph
- high in K+
- low in Na+
- K+ higher than CSF of hair cells
- -> only place in the body this occurs
tectorial membrane
stationary
hair cells
- mechanoreceptors
- easily damaged by intensity noises (concerts, jet engine, construction equipment)
- can also be damaged by chronic exposure to low intensity
primary auditory cortex
temporal lobe
inferior collculus
midbrain (reflexive movements of head)
how many tastes can a human distinguish?
about 10,000
how many sounds can a human distinguish?
about 400,000
how many tastes can a human distinguish?
perceive hundreds
static equilibrium
perception of orientation of head when stationary
dynamic equilibrium
perception of motion/acceleration
types of dynamic equilibrium
- linear acceleration
- angular acceleration
linear acceleration
change in velocity in straight line
angular acceleration
- “rotational equilibrium”
- change of rate of rotation
vestibule
- utricle
- saccule
utricle
horizontal plane
saccule
vertical plane
utricle and saccule
Brain interprets orientation of head by comparing input from both:
- – static equilibrium
- – linear acceleration
otoliths
ear stones
where are otoliths?
embedded in gelatinous fluid
- when head position is changed, fluid bends hair cells
semicircular ducts
- angular acceleration (rotational equilibrium)
- detect rotation in 3 different planes
- – “yes”
- – “no”
- – “lateral”
vestibuloobular reflex (VOR)
rotate in equal/opposite direction to “keep eye on target”
light
- electromagnetic radiation
- visible light (400-700nm)
- detected by photoreceptors
- -> rods and cones
neutral tunic contains
- retina
- fovea centralis
retina
photoreceptors
fovea centralis
increased concentration of photoreceptors
- image focused here
- high concentration of cones
fibrous tunic contains
- sclera
- cornea
sclera
connective tissue outer layer
cornea
clear anterior surface
- bends light rays most
vascular tunic contains
- choroid
- iris
- ciliary muscle
choroid
pigmented vascular layer
iris
muscles control diameter of pupil
ciliary muscle
change shape of lens
rest of the eye
movement and focusing imaging
tunics
fluid-filled ball
refraction
light bends
lens
fine tunes
- can change shape with ciliary muscles to focus light on retina
accommodation
change curvature of lens to focus on near objects
- shape of lens controlled by ciliary muscle
- -> parasympathetic control
distant vision
- ciliary muscle relaxed
- suspensory ligament taut
- lens thins
near vision
- ciliary muscle contracted
- suspensory ligament relaxed
- lens thickens
pupillary constriction
to help focus light rays, the iris changes the pupil size to regulate amount of light that enters the eye
- makes edges of image clearer
pupil dilated
sympathetic effect
pupil constricted
parasympathetic effect
myopia
nearsightedness
- can’t see objects far away clear
nearsightedness
eyeball too long
nearsightedness corrected
concave lens diverges light rays
hyperopia
farsightedness
- can’t see objects close up
farsightedness
eyeball too short
farsightedness corrected
convex lens converges light rays
optic disc
- blind spot
- no photoreceptors here
- where axons converge to become optic nerve (lots of blood flow)
visual filling
brain “fills in” information based on background
pigment epithelium
absorbs stray light
- no reflection
bipolar cell
produce graded potentials
- no action potentials
horizontal / amacrine cell
modify signal using lateral inhibitor to enhance contrast
ganglion cell
- action potentials
- axons of ganglion cells from optic nerve (CN II)
- true neurons
rods
- respond in dim light
- located in periphery (alert us to motion)
- high sensitivity
- low acuity
- no color vision (black and white)
cones
- respond in bright light
- dense around fovea
- high acuity (sharp image)
- low sensitivity
- color vision
outer segment of rod/cones
contains photopigments
inner segment of rod/cones
organelles
night vision
many rods converge to stimulate one ganglion cell
- large receptive field
- up to 100 rods / bipolar cells
spatial summation of night vision
- increase sensitivity
- decreased resolution
day vision
each cone has a ‘private line’ to the brain
- small receptive field
- increased resolution
- decreased sensitivity
- NO summation
photopigments: rods
rhodopsin
photopigments: cones
photopsins
cone has 1 of 3 types of photopsin:
- S (blue) cone
- M (green) cone
- L (red) cone
blue light
benefiting during daylight hours
- boost attention, reaction times, and mood
- suppressed melatonin for about twice as long as green light and shifted circadian rhythms by twice as long
what color should the numbers be for an alarm color?
red
red light
has the least power to shift circadian rhythm and suppress melatonin
signaling in the dark process
- cGMP is high –> cation channels open
- rod cell is depolarized - glutamate is released onto bipolar cell (IPSP)
- bipolar cell hyperpolarizes
- no excitatory neurotransmitter released onto ganglion cell
- No action potentials to brain
rhodopsin
GPCR (opsin) + retinal (form of Vitamin A)
retinal
light sensor
visual signal transduction pathway
- rhodopsin absorbs photon of light
- Cis-retinal isomerize to trans-retinal
- - causes conformational change in opsin - opsin triggers reaction cascade that breaks down cGMP
signaling in the light process
- cGMP levels falls –> cation channels close
- - rod cells hyperpolarizes - no glutamate is released onto bipolar cell
- bipolar cell depolarizes
- excitatory neurotransmitter released onto ganglion cell
- action potentials to brain via CN II
dark adaptation
when moving from bright light to dark
- rhodopsin was bleached in light
- takes about 5 min to regenerate 50% of bleached rhodopsin
- 20-30 min for max sensitivity
light adaptation
- when moving from dark to bright light
- rods all become bleached because image is too bright
- poor contrast
- adaptation occurs quickly
lateral inhibition
- horizontal cells
- amacrine cells
ON bipolar cells
- depolarize (no glutamate from rods)
- release NT –> stimulate ganglion cell to have AP
OFF bipolar cells
- hyperpolarize (and glutamate)
- no NT release
- no AP ganglion cell
