7- The Other Senses Flashcards
Inner ear
Oval window, cochlea, basilar membrane, auditory nerve, round window
scala vestibuli, scala tympani, scala media
hair cells, cochlear neuron, techtorial membrane, basilar membrane)
Outer ear
Pinna (flesh and cartiledge alters reflextions of sound waves to locate sound)
external auditory cannal
Place theory
each area along basilar membrane tuned to specific frequency, each activates hair cells of one place along membrane
-NS distinguishes based on which neurons respons
But- some parts of membrane bound to tight for this
Frequency theory
basilar membrane vibrates in synchrony wt a sound, auditory nerve axons potentiate at same frequency
But- maximum firing rate of neuron = 1000 hz (and we hear up to 20,000)
Theory of hearing now
Frequency theory for low frequencies
Volley principle for up to 4000 hz
Place theory for above 4000
Auditory cortex
Auditory cortex, medial geniculate, inferior colliculus, superior olive, cochlear nucleus
Primary audiotry cortex (A1) superior temporal cortex (auditory imagery) -damage does not mean deafness, but inability to recognize sequences of ound
Areas outside A1 for auditory ‘objects’
anterior temporal cortex = what pathway
posterior temporal cortex + parietal = where pathway
Conductive/middle ear deafness
sometimes temporary or correctible wt surgery/hearing aids
-hear self clearly
Nerve/ inner ear deafnes
damage to cochlea, hair cells, or auditory nerve
- hearing aid only if receptors lost in cochlea
- nerve damage = prenatal exposure to rubella, syphillis, decrease o2 during birth
-nerve deafness
= Tinnitus (ringing in ears)
Sound localization
difference in intensity btw ears = sound shaddow (2000-3000 hz)
- difference i time of arrival
- phase difference (2 consecutive peaks 360 degrees apart, up to 1500 hz)
Vestibular Organ
When head tilts calcium carbonate Ololiths that lie next to hair cells push against/excite them
- semicircular canals filled wt jelly & lined wt hair cells
- acceleration of head causes jelly to push against hair cells
- action potentials travel to brainstem and cerebellum
Somatosensory system
shape of an object = descriminative touch
-deep pressure, temperature, pain, itch, tickle, position/movement of joints
-stimulation of touch receptors open Na channels in axon = AP
Chemicals stimulae receptors for heat/cold
Skin receptors
Free nerve ending (pain, warmth, cold)
Hair follicle receptors (moving hairs)
Meissner’s corpuscles (sudden displacement of skin)
Pacinian corpuscles (sudden displacement of skin, high freq vibrations)
RUffini endings (stretch)
Krause end bulbs (uncertain)
itch
mild tissue damage = histamines = itching
contact wt some plant
- some axons for histamine, some for plant itch (also respond to heat)
- activate neurons to produce gastrin-releasing peptide
opiates increase
scratching = pain decreases
Pain
prefrontal cortex
capsaicin - burning/stinging
- bare nerve ending receptors- slow conduction (motor responses faster than touch) - axons release NT in spinal cord (mild- glutamate, strong- glutamate and substance P)
- spinal cord- ventral posterior nucleus of thalamus- somatosensory cortex
or
-reticular formation of medulla - central nuclei of thalamus - amygdala and hippocampus - prefrontal cortex - cingulate cortex
= emotional associations of sensations
Pain relief
Opioid mechanisms- systs that respond to opiate drugs and similar chemicals to receptor in spinal cord and periaqueductal grey area (midbrain)
=block release of substance P
Endorphins- decrease pain (B-endorphin)
But- dynorphin A increases pain
(more in inescapable pain, during sex, thrilling music
less in brooding)
estradiol in females facilitates opiate activity
Gate theory
spinal cord neurons receive messages from pain receptors and touch receptors and from axons descending from brain
other inputs close gates for pain messages
Pain relievers
Morphine - blocks slow dull pain after surgery
Placebo- no pharmacological effects
cannabinoids- block some pain in periphery of body, not CNS
Capsaicin- releases substance P faster than neurons resynthesize it= less able to send pain message (high doses damage pain receptors)
-topically or to blood stream
electrical stimulation of NS (in Thalamus or by pain pathways in spinal cord)
Inflamed tissue
release histamine, nerve growth factor, other chems
increase response by heat and pain receptors
decrease wt ibuprofen
-chronic pain after injury due to increased response to same input
Labeled-line principle
Across-fiber pattern principle
Labeled-line principle- each receptor responds to limited range of stimuli, meaning depends on which neurons are active
Across-fiber pattern principle- each receptor responds to a wider range of stimuli and a given response by a given axon means little except in comparison to what other axons are doing
Substances that modify taste receptors
Miraculin (acids stimulate sweet)
sodium loryl sulfate (toothpaste)
gymnema sylvestre (dont taste sweet)
Adaptation
Cross adaptation
a: fatigue of receptors sensitivity to certain tastes
ca: reduced response to one taste after exposure to another
Salty, sweet, sour, bitter, umami
dif rhythms of action potentials in taste sensitive part of medulla
salty allows sodium ions through membrane on tongue
sour detects acids
sweet, bitter, umami- when molecule bingds activates g protein, which releases second messenger
neurons respond to 2+ kinds of taste
25+ bitter receptors
NIS - nucleus of the tractus solitarius
in medulla
info branches to pons, lateral hypothalamus, amygdala, ventral-posterior thalamus
+ somatosensory cotex
+Insula (primary taste cortex)
VNO Vomeronasal organ
set of receptors near olfactory receptors respond only to pheromones
1 receptor per pheromone
Middle Ear
Tympanic membrane, hammer, anvil, stirrup
