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PHYL 2041 > Final > Flashcards

Final Flashcards

1
Q

3 parts of the cerebral hemispheres

A

Cortex (surface)

white matter (nerve tracts)

deep structure (basal ganglia, anygdala and hippocampus)

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2
Q

commissures

in the hemispheres

A

Commissure are nerve bundles

the largest is the corpus callosum

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3
Q

Topographic organization in the brain

A

each area of the cortex is organized topographically

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4
Q

ipsilateral/contralateral organization in the brain

A

most of the brain is organized conralaterally, but the cerebellum is organized ipsilaterally.

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5
Q

physical structure of the cortex

A

Most of cortex is 6-layered with large pyramidal cells - Betz Cells - whose axons make up the major output

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6
Q

Brodmann areas

A

52 regions of the brain

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7
Q

neocortex, archicortex and paleo cortex

where is the hippocampus?

where is the cingulate cortex?

A

are phylogenetically older areas of the brain.

Have less layers of cells (3, 4/5)

90% of human brain is the newer neocortex

archicortex contains the hippocampus

cingulate cortex is part of the paleocortex

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8
Q

The cortexes and their functions

A
  1. Occiptal - vision
  2. parietal - somatosensory
  3. temporal - hearing, language, speech
  4. frontal - motor and general planning
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9
Q

Association areas of the brain

A

large areas, particularly in the frontal and parietal lobes that are assumed to be for higher function

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10
Q

overrepresentation in the somatosensory cortex

A

Some areas in the somatosensory cortex that are important for touch sensation are overrepresented on the topographic map of the cortex

these areas have higher two point discrimination

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11
Q

Phantom limbs

A
  • When part of the body is lost, it’s corresponding region of the sensory homunculous still exists
  • plasticity leads to other parts of the body connecting with this region, so sensation in those regions may lead to sensation on the phantom limb
  • May be painful/unpleasant
    *
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12
Q

Common causes of prolongued pain (6)

A
  1. Shingles = postherpetic neuralgia. Reactivation of zoster virus can leave pain for months or years
  2. Tic Douloureux = trigeminal neuraliga. Intense facial pain. Due to pressure on the trigeminal by vascular or neuroplastic changes
  3. Cancer pain - tissue damage activates silent nociceptors
  4. Spinal nerve root compression - eg herniated disk
  5. fibromyalgia - widespread pain in muscles, joints, bones without known cause. More in women
  6. Complex regional pain syndrome - usually an entire arm or leg.
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13
Q

Central pain:

Damage to anterolateral disk

Damage to thalamus

A

Damage to the anterolateal system can cause central pain. Particularly on the spinothalamic and spinoreticular fibres.

Damage to thalamus itself can lead to central pain.

Central pain can be intense and can involve half of the body. Often resistant to analgesics.

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14
Q

Effect of distraction on pain

A

Many people don’t feel pain in urgent activites

Dstraction reduces percieved pain

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15
Q

Responses to pain: somatic reflexes

A

due to spinal cord connections

Flexor and crossed extensor reflexes - cutaneous pain in an extremity causes limb withdrawal and contralateral limb extension

scratch reflex - cutaneous pain on the body causes limb to remove the source of irritation.

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16
Q

Responses to pain

  • autonomic responses
  • emotional responses
  • learning and memory
A

hypothalamus and brainstem

  • Increased heart rate, respiration rate and blood pressure
  • Nausea, vomiting, sweating, dilated pupils

cingulate cortex and limbic system

  • anxiety, fear

hippocampal connections

  • Important to learn to avoid pain, but people can learn to expect pain, which increases perception of pain (wind up phenomenon)
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17
Q

EEG

what is it

records

wave types

used clinically for

contaminated by

A

electroencephalogram

  • small ascillating voltage recorded from the scalp.
  • Mainly measures post synaptic potentials produces by thalamic signals to the cortex
  • Alpha rhythms when we are relaxed, awake, eyes closed
  • Beta rhythms when open eyes, alert, even in dark. Smaller and faster than alpha.
  • Used clinically because epileptiform (abnormal) EEG shows off electrical activity in the brain and can be used for diagnosis of epilepsy, coma level and brain death, measurement of anaesthesia effects, detection of psychotropic drugs
  • EEG can be contaminated by eye movements, tongue movements, EKG
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18
Q

REM sleep

when

waves look like

cycling

amount of REM

physical symptoms of REM

A

At the end of the first sleep cycle, the person doesn’t wake up, instead they enter into REM

REM looks similar to normal/awake/alert EEG

after a short time anodhter cycle through stages 1-4 occurs

Amount of REM increases with each cycle

REM is usually 4 times per night about 20-25% of the total sleep time

When dreaming occurs; muscles relaxed, eyes frequently active, twitches of muscles

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19
Q

Parasomnias

  1. Somnambulism
  2. Night terrors
  3. rhythmic movement disorder
  4. REM behaviour disorder
  5. Restless leg syndrome
A
  1. Somnambulism - sleepwalking and sleeptalking but not dreaming. Can’t see; often injured
  2. Night terrors - screaming, sweating, frightened, more than nightmare
  3. rhythmic movement disorder - rocking, head-rolling
  4. REM behaviour disorder - acting out dreams, can cause injury to sleeper or companions
  5. Restless leg syndrome - involuntary leg movements; genetic links
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20
Q

treatment for severe sleep disorder symptoms

A

tranquilizers - benzodiazepines

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21
Q

NT release during sleep and wakefulness

A

During wake/alert state, neurons that release norepinephrine and serotonin are active

During awake or in REM sleep, neurons that release acetyl choline are active

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22
Q

sleep wake cycle driven by

A

Circadian rhythm - a clock mechanism inherent to the brain and triggered by night/day cycle

sleep/wake cycle influenced by several areas of the brain

  • superchiasmatic nucleus
  • hypothalamus
  • reticular system
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23
Q

coma

A

means a person cannot be aroused

result of many causes (injury, disease, drugs)

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24
Q

consciousness

includes

brain regions

paying attention

A

includes self awareness, thought, decision making, feeling, planning, imagining

structures involved in consciousness are not well know. Parts of cerebral cortex: thalamus, basal ganglia are essential

the ability to pay attention is enhanced by sensory information

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25
Q

right parietal damage

A

leads to loss of awareness of the left visual field and body parts on the left side.

The opposite occurs for left parietal damage

hemi-spatial neglect

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26
Q

apraxia

A

difficulty performing complex motor tasts due to premotor cortex, corpus callosum, parietal cortex damage

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27
Q

schizophrenia

type of disorder

causes

includes

treatment

A

a disorder of consciousness

Due to a variety of causes including genetic predisposition

delusions, hallucinations, often paranoia

helped by dopamine antagonists

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28
Q

general mood disorder treatment

treatment for bipolar disorder

A

Drug therapies for mood disorder usually increase serotonin or norepinephrine by limiting reuptake or degredation

  • most popular increase serotonin - prozac

Lithium effective for damping mood swings in bipolar disroder. Mechanism probably involves second messenger systems

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29
Q

Frontal lobe

functions

size

age of maturity

types of neurons

result of damage

A

Impulse control, judgement, language, working memory, motor control, sexual behaviour, socialization, spontaneity, planning, coordination

  • Executive functions: recognizing future consequences of actions, choosing between good, bad and better actions, suppressing unacceptable social responses, determining similarities and differences between things or events

developed later in evolution. Enormous in humans and relatively high in apes.

reach full maturity around age 25

rich in dopamine sensitive neurons

Damage leads to: impulsiveness, impaired planning of complex action sequences, persistence when change would be more appropriate

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30
Q

limbic system:

what does it mean

includes

major functions

function of the amygdala/result of damage

A
  • LImbic means edge/border so its contents are the inner edge of the cingulate cortex
  • Includes amygdala and hippocampus and thalamus (thalamus and front lobe are often included)
  • Major function is emotion, control of hypothalamus, learning/memory
    • Amygdala important for expressing emotion and interpreting emotion in others
    • Stimulation produces sensations of fear/apprehension
    • Amygdala is selectively activated by expressive faces
    • Damage leads to inability to detect emotion in others
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31
Q

Papez circuit

A

originally thought to be mainly concerned with emotion

now considered to be important for memory

important cerebellar inputs

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32
Q

Hypothalamus

where is it

important for

involved in controlling (long list)

A

Small structure under the thalamus

Connected to pituitary gland

Important for homeostatic control - receives inputs from many sensory structures throughout the body and compares them to optimal set points

involved in controlling: anterior pituitary gland, blood pressure, water balance, eating and drinking, reproduction, circadian rhythm, body temperature, emotional expression, general autonomic functions

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33
Q

Thermoregulation

A

Pyrogens change the hypothalamis set point causing fever

Central heat receptors in hypothalamus detect changes

Shivering activaes muscles - piloerection (raised hairs)

Too much heat - sweating and blood flow to surface of skin to cool off

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34
Q

Two major classes of memory

A

Declarative: factual information (phone numbers, faces).

Procedural: how to do things like skating/riding a bike

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35
Q

forming declarative and procedural memories

limit to memory

damage to hippocampus

lateral specialization of hippocampus

A

Hippocampus is critical for forming long-term declarative memories

Cerebellum is involved in forming procedural memories

Seems to be no limit to the amount of declarative memory

Damage to hippocampus prevents storage of long-term memory, but does not erase existing memory

Lateral specialization of hippocampus:

  • left = verbal memory, learning
  • right = spatial memory
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36
Q

Cellular basis of memory

A
  • Memory involves synaptic strength
    • changes in amount of NT released with AP
    • changes in size of PSP produced by a fixed amount of NT
  • 2 models
    • Long term potentiation and long term depression.
    • Synaptic connections become stronger or weaker after appropriate stimuli and remain unchanged for days or weeks
  • changes in 2nd messenger systems are particularly important
  • Growth of postsynaptic reions or neurons or the delivery of additional receptor molecules to the postsynaptic membrane
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37
Q

Cerebral hemisphere specialization and dominance

corpus callossum cut studies show

specializatation of left and right

sominance

A
  • Studies with a corpus callossum cut show that the two hemispheres can operate relatively independently and disagree about what to do
    • Alien hand syndrome - one hand acts indpendently of conscious thought
  • Language concentrated in left - speaking, writing and understanding language
  • Left tends to dominate brain activity
  • right hemisphere specializes in spatial functions: perspectives of 3D objects, recognizing faces, mathematical skill, but can understand simple language too
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38
Q

hemisphere that recognizes an object

Implications in split brain

A

Objects in the right visual field will be perceived by the left brain only and vice versa.

A split brain patient’s hemispheres can’t communicate so when a word or image appears in the left, the info goes to the right brain and the patient can’t name it, though they can draw it.

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39
Q

Broca’s and Wernicke’s areas

describe. Result of damage to each

connected by. Damage to this

A

Broca’s area = creation of speech, using respiratory muscles, vocal chords, mouth (left hemisphere)

  • damage causes expressive aphasia

Wernicke’s area = Language comprehension, musical tone comprehension, non-verbal sounds

  • Damage causes trouble understanding spoken or written speech. People may produce fluent but meaningless speech

The two areas are connected by the arcuate fasciulus - damage to it causes difficulty repeating words: conduction aphasia

  • You would have to hear the word, understand it and then have it repeated in Broca’s area
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40
Q

language: damage to central areas

A

leads to more difficulties in language comprehension - central aphasias

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41
Q

Sclera

Aqueous humour

vitreous humour

lens

cornea

choroid

fovea

A

Sclera - the white over the whole eye

Aqueous humour - under the cornea

vitreous humour - filling up most of eye

lens - the disk at the front of eye

cornea - protective layer over the pupil and lens

choroid - dark structure behind the retina. Dark in humans because all light is absorbed. Not for nocturnal animals

fovea - depression at the back of retina. fine focus

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42
Q

Cornea

A

transparent, convex structure

Non-vascular

many nerve endings - trigeminal nerve (so very sensitive to touch)

Light coming in has to be bent - 2/3 of total focusing power

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43
Q

Pupil

what is it

why black

size controled by

increases depth of focus as

analogous to

A
  • Hole at the centre of the iris.
  • Appears black because all light entering the eye is absorbed
  • Size controled by radial and circular eye muscles
  • Pupil increases depth of focus as it becomes smaller due to pinhole effect
    • light from one part of object only reaches one part of the eye (due to pinhole)
  • directly analogous to a camera aperture - more depth of focus with more available light
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44
Q

pinhole effect

A

LIght from one part of an object only reaches one part of the eye due to the pinhole

Distance of object from pinhole doesn’t matter - still get a sharp image/depth of focus

smaller pupil = better focusing on back of eye

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45
Q

Iris

colour

muscle control

A
  • Has pigmented cells containing several types of melanin, another pigment is lipofuscin
  • Number and position of pigment cells leads to eye colour
  • Iris has blood vessels so haemoglobin in blood contributes to colour
  • Eye colour is difficult to predict even if genetics are known
  • Two groups of muscles: sphinchter/circular muscles constrict the pupil and radial muscles dilate the pupil.
  • Iris muscles controlled by autonomic system: sympathetic drive radial (dilate), parasympathetic drive circular
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46
Q

pupillary light reflex

A

Light falling in eye causes reflex activation of circular muscle.

Light detected by retina - signal goes from eye to pretectal area of midbrain and then back to ciliary ganglion of parasympathetic

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47
Q

Lens

what does it do

how does it do it

far-sighted

A

Adjusts focus

Distant vision - thin, stretched by zonule fibres

Near vision - circular ciliary muscles contract, allowing lens to relax

Only activates focusing power on far things. As we age, the lens gets rigid and won’t relax as easily so near vision is compromised (far sighted)

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48
Q

accomodation and vergence

A

As an object moves farther and closer, the lens must change shape - accomodation - to maintain focus

For a close object, eyes converge (turn in). Degree of convergence is used by brain to determine how far or close the object is. - binocular depth cue

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49
Q

cataracts

A

Clouding of the lens due to protein changes

mostly age-related

lens colour also changes

Surgical removal is common procedure - lens replaces with a prosthetic implant. Restores vision, but accomodation is lost because the lens has fixed depth focus

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50
Q

Aqueous and vitreous humours

A

Lens seperates the eye into two chambers. Aqueous humour fillst he front and the vitreous humour fills the back

Vitreous humour occupies 2/3 of eye and is a jelly like consistency and transparent.

Vitreous humour naturally shrinks with age and tends to seperate from the retina giving the appearance of floaters are the vitreous pulls away causing visual phenomena

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51
Q

Glaucoma

A
  • Aqueous humour is clear, filling the frount of the eye
    • Produces by the epithelium of cilary body; flows through pupillary space and exits through Schlemm’s channel
    • Carries nutrients to the cells of the lens and cornea
  • Conduction and drainage of aqueous humour controls intraocular pressure (IOP)
  • Glaucoma is a common eye disease that is associated with elevated IOP, though some glaucoma patients have normal IOP levels
  • Causes damage to optic nerve
  • Produces loss of peripheral vision (visual world starts to shrink), but is not usually noticed until there is already signficant damage
  • Surgery to make additional hols is done if Schlemm channel is blocked
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52
Q

Retina

A

choroid absorbs most of the light

the macula (darker area) contains the fovea, where accurate vision occurs.

Blod vessels avoid the macula/fovea so as not to interfere with vision

the blind spot is the area of the visual field correspondng to the optic disk - no retina there but the brain can fill in missing info for colours, lines, patterns (each eye has diff blind spot so they fill in for each other)

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53
Q

optic disk

A

where the optic nerve and the blood vessels leave and enter the eye

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54
Q

Light

A

A photon is a single quantum of light with energy -hc/wavelength

Natural light intensity range from brightest to darkest is 10^15, human functional intensity is about 10^12 with time for adaption

Human short term functional intensity about 10^3

Longer wavelengths = lower energy. A lot of animals can see beyond 400 nm but we can’t

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55
Q

Retinal cells

A

ganglion cells

amacrine cells

bipolar cells

horizontal cells

rods and cones

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56
Q

retinal cells distribution

A
  • rods and cones > bipolar cells > ganglion cells
  • amacrine cells connect bipolar cells
  • horizontal cells connect rods and cones
  • Foveola - mashed with cones. Each cone to a ganglion cell
  • Fovea - depression in macula; mainly cones, fewer as you move away
  • periphery - outside macula; manily rods, few cones; up to 250 rods per ganglion cell
57
Q

Rods structure

A
  • Rhodopsin is a light sensitive molecule on disks (photopigment/visual pigment)
  • Disks are made by invagination of epithelium. Made hourly and progress down the rod, eventually being degraded at end
  • First few rods are clear invaginations, and then they move down and separate
58
Q

cones structure

A
  • much less in eye than cones
  • Disks are all invaginated from the epithelium and remain that way. Cone shaped
  • In some animals (not humans), you find oil droplets full of brightly coloured pigments
59
Q

retinitis pigmentosa

A

a group of at least 70 different genetic diseases in which the retina degrades

some cause rod/cone degeneration, some due to failure of pigment epithelium to degrade disks, causing accumulation of debris

60
Q

Rhodopsin structure

A

Rhodopsin is made up of opsin and retinal

  • Retinal absorbs light (in UV too)
  • Opsin has 7 TM helices, determines the wavelength of absorption of light and has retinal in it
  • Retinal is derived from vitamin A - has a highly conserved molecular structure
  • Retinal is surrounded by amino acids (opsins) that shift vibration frequencies of double bonds in retinal, giving different light absorption wavelengths
  • OPsins shift the retinal absorption into the visible wavelength - depending on what the opsin is, we see a diff shift int he visible region
  • Humans have 4 opsins: red, gree, blue cones, plus rods (mainly green)
61
Q

Transduction in rods

A
  • Light hits rhodopsin, causing it to change to meterhodopsin
  • Metarhodopsin has a chemical cascade that reduces cGMP concentration
  • cGMP normally holds the Na channels open when there is darkeness - dark current
  • Light lowers cGMP and closes Na channel, so that receptor potentials are hyperpolarizing
62
Q

Ion current in rods

A
  • cGMP opens Ca/Na channel that is primary sodium selective but some Ca gets in too.
  • In light, cGMP is downregulated and this channel is closed
  • Na and Ca levels are dealt with bu the Na/Ca exchanger and the Na/K pump to keep Ca levels low
  • Ca is important for adaption process
63
Q

Light adaption

A
  • With dtrong light, the amount of rhodopsin available falls to about 1% of normal. This reduces sensitivity but cannot account entirely for major adaption to light.
  • Ca important for light adaption
  • Adaptopn much faster to light than to dark
  • Rods adapt more than cones, but cones adapt more quickly
64
Q

Temporal resolution of fovea

critical fusion frequency

A

Critical fusion frequency = the frequency at which a flashing image beinfs to look continuous (used for movies)

65
Q

Horizontal cells important for

A

collecting information from surrounding area

66
Q

processing in retinal cells

transduction in rods/cone and bipolar cells

amacrine cells

retinal processing favors in different light

A
  • These first two layers of retinal cells don’t use APs
  • The distance is so small that graded potentials can propogate without much loss
  • 2 types of bipolar cell responses - due to different synaptic receptors to the same transmitter (glutamate)
  • amacrine cells perform a great deal of processing before visual signals leave retina via optic nerve
  • Retinal processing favors fine discrimination in bright light and maximum sensitivity in dull light
  • visual receptive fields are split into centre and surround - each with different effects on the cell.
67
Q

receptive field

A

is usually the area on the retina where light causes a change in activityin the neuron

light falling on other parts of the retina has no effect

neuron may be far from the receptive field (in visual cortex)

receptive field split into centre and surround

68
Q

Retinal ganglion cell responses: centre and surround

A

Surround is the ‘off region’ - fires less in light and demonstrates an ‘off burst’ when light is turned off

centre is the ‘on region’ - fires less in darkness, ‘on burst’ when light is turned on

If both are illuminated together, little to no response on ganglion cell

dark adaption can make both areas excitatory in darkness

light outside of these regions has no effect on the neuron

primate fovea centre are less than 0.1 mm - larger in cats

69
Q

Intrinsically photosensitive retinal ganglion cell

function

structure

transduction mechanism

connected to

A
  • ganglion cells that can detect light without rod or cone input.
  • Stillconnected to bipolar and amacrine cells that respond to rod and cone inputs
  • large dendritic areas containing melanopsin - blue-sensitive photopigment
  • different transduction mechanism - IP3, not cGMP
  • slow responses - measure average ight level
  • connected to superchiasmatic nucleus - important for light/dark cycle behaviour
  • Involved in release of melatonin from pineal gland
  • Can contribute to conscious vision, though probably low acuity
70
Q

overlap of ganglion cell receptive fields

A

half have ‘on’ centre, ‘off’ surround, the outher hald have the opposite

ganglion recpetive fields overlap on the retina

Alignment of different receptive fields is probably to help detect light/dark edges

71
Q

two levels of crossing over in vision

A

Light crosses over in the eyes, so nasal visual fields go to temporal retinas and temporal visual fields go to nasal retinas

Axons from nasal retinas cross at optic chiasm

72
Q

retinal topographic organization

A

Topographic at each level, but distorted in favour of fovea

distorted because there are so many retinal ganglion cells in the fovea

points that are next to each other on the retina, tend to have axons leaving together

73
Q

lateral geniculate

A

lateral geniculate nucleus of the thalamus

inputs fromt he two eyes are still separated here

receptive field is similar to that of ganglion cell with on/off centre/surround

74
Q

Damage to optic chiasm

A

retain central nasal vision, but you see a narrower world

75
Q

subcortical retinal ganglion pathways

A

paths leaving the retina that don’t end up at top of midbrain like most others.
to superior colliculous and pretectal area (brainstem)

76
Q

superior colliculus

A

subcortical visual destination

superior colliculous has topographic map and matching maps of auditory and other sensory modalities

  • recieves input from cerebrum
  • controls saccadic eye movement
  • contributes to blindsight - can’t consciousless see, but aware of surrounding
77
Q

pretectal area

A

subcortical visual destination

pupillary reflex - light entering eyes is used to determine diameter of pupil

78
Q

overrepresentation of fovea in the cortex

macula sparing

A

fovea is overrepresented in the thalamus and cortex - even has dual blood supply to areas in the cortex representing fovea

damage to cortex usually results in loss of vision in the corresponding visual field.

Loss of peripheral vision is common, but some maintain vision from the fovea because it is represented in such a large portion of the cortex

79
Q

Simple cortical neurons

A

Have receptive fields with centre/surround organization, but distorted to respond better to lines

80
Q

complex cortical neurons

A
  • more numerous than simple cortical neurons, larger receptive fields, respond better to bars or edges of a particular orientation
  • use convergence from simple cells
  • we seem to analyze the visual world based mostly on lines.
  • Cortex organized into groups of cells responding to different orientations of lines
  • more complex shape = more complex cells repsonding
81
Q

columnar organization

A

at any point in a vertical column, the cells have a similar type of receptive field orientation.

82
Q

ocular dominance

A

Many cells respond to inputs from either eye, but there is ocular dominance - a strong response to one eye for each column

83
Q

colour receptors in humans

A

red, green and blue

84
Q

opsin mutations

A

has complex molecular biology

two important genes for opsins on X chromosome so red/green blindness if common in men

some people lack colours (like green), other have mixed up hybrids due to deletions and duplications

85
Q

Colour in retinal ganglion cells

result of damage

A

M and P cells.

M cells are not colour sensitive

P cells (80%) are composed of red/green opponents, and blue/yellow opponents

damage to colour pathways can selectively remove colour sensations from part of visual field leaving only black and white vision in that area

86
Q

human frequency sound range

sound location

A

20-20,000 Hz

Higher Hz = shorter wavelength

location of sound mainly detected by time delay between the sound arriveing at each of the two ears

sound location impossible at low frequencies

closer ears means you need higher frequencies to do sound location

87
Q

Eustation tube

problems with pressure

A

COnnected to the back of the throat, but entrance is clsoed except for in yawning and swallowing

middle ear is normally at atmospheric pressure, so this is problematic when going up in planes. You need to open you eustachian tube to normalize pressure. Conscious action.

88
Q

trasduction of sound in middle ear

A

eardrum > malleus > incus > stapes > oval window

middle ear transmits sound from air to water because coclea is filled with endolymph

when sound hits air/water interface, about 99% is reflected

contraction of muscles reduces sound transmission

  • acoustic reflex: lous sound causes muscle contraction
89
Q

audiometry

A

the measurement of auditory system function. Measure minimum sound pressure for detection at different frequencies

hearing loss is usually due to damage to middle ear or the cochlea

presbycusis is loss of hearing (especially high frequencies) with age

weber test tests bone conduction through middle ear. Knock head, shoul hear equally in both ears

rinne test - compares sound and air conduction in one ear. Place tuning fork next to mastoid bone and tell patient to tell you when they stop hearing it. When they do, hold it outside pinna and ask if they can hear it. They should because air conduction is longer than bone conduction

90
Q

wave travel in cochlea

A

waves grow in amplitude as they travel down basilar membrane.

Gap at end of basilar membrane called helicotrema

travelling wave has an enveloped maximum displacement that changes with frequency

peak or the envelope moves down the basilar membrane has we go from high to low frequency

91
Q

auditory neuron thresholds

A

basilar membrane pushes hair cells against he tectorial membrane

hair cells transduce movement and synpase onto auditory neurons

threshold intensity changes with each frequency specialization.

Each neuron responds becast the frequency it was meant for. Depending on its position on the basilar membrane, that is where that preferred frequency envelope is at max displacement

helicotrema likes low frequency, by stapes is high frequency

92
Q

Inner and outer hair cells

A

3 rows outer hair cells

1 row inner hair cells

inner hair cells transduce movement into graded membrane potential changes. Have no axons, but synapse onto neurons that send APs along axons into auditory nerve

outer hair cells contract with depolarization, as well as transduce movement. Contract with music.

93
Q

cochlear amplification

A

cochlea has great sensitivity that depends on local amplification mechanism

can tell that it amplifies because the ear itself often makes sounds

outer hair cells may give feedback to amlify guiet sounds and negative feedback to reduce loud sounds

94
Q

organization or auditory cortex

damage

electrication stimulation

A

Organization if tonotopic at each level - large and complex map of sound frequency in human cortex

damage to cortex causes more deafness in contralateral ear, but not complete deafness because of complex crossing over

electrical stimulation of cortex gives sensation of sounds

95
Q

organ of corti

A

on basilar membrane

stimulated by vibrations and sends nerve impulses via hair cells

96
Q

hair cell potentials (1)

A

hair cells use graded potentials to synapse onto neurons

97
Q

Membranous labyrinth includes

A

includes membranes lining bony labyrinth

98
Q

sensory nerves leaving vestibular system

A

leave each of the canals and the big chambers.

join to form the vestibular nerve - 8th cranial nerve

99
Q

functions of vestibular system

A

control of eye, head and body positions

spatial sensation

ditinguish between velocity, force and angular movement

100
Q

vestibular system experience of acceleration due to gravity

A

detects acceleration, not velocity. If you sit on a plane and it’s not accelerating you don’t feel movement

Cannot distinguish between gravity and acceleration upward - so you just feel heavy when going up an escalator

101
Q

Otolith organs

A

Stones in the ear

density 3:1 endolymph

detect linear acceleration by moving to fall and sitmulating hair cells in saccule and utricle.

hairs in utricle and saccule bend preferentially

In utricle, horizontal respons inward

In saccule, vertical respons where hairs bend away from the striolla

102
Q

detecting angular acceleration

A

Inside the ampulla is the cupulla, that bends in response to pressure, moving hair cells one way or the other depending on which way the endolymph is trying to move.

any movement that causes the endolymph to move relative to the canal will bring about a circular motion response.

103
Q

ampulla response to acceleration in firing

A

ampulla fires all the time, fires more when accelerating and less when decelerating

104
Q

vestibular neural connection

A

very fast connections to cerebellum and vetibular nucleus or spinal cord

cranial nerves 3, 4, 6

105
Q

saccades

A

quick changes in fixation point ar normal and continual

if the eye is artificially fixed, the image washes out.

106
Q

saccadic and tracking vision

contributions to normal vision

ouchi illusion

vestibular-ocular reflex

A

normally, vision includes a mixture of saccadic and tracking movements. Tracking if an opbject of interest that moving across the visual field or subject moves relative to visual world

Ouchi illusion - horizontal sacades make the disk appear to move and vertical make background apear to move so disk looks floating

vestibular-ocular reflex - in angular acceleration, subject will make slow tracking movements and when their fixation point is out of view, there is fast saccades to track that object again

107
Q

vestibular nystagmus

A

rotation of the head (even in dark) results in repeated slow tracking movements in opposite direction

displays plasticity - can change amplitude and direction if the eyes are fitted with prism glasses

108
Q

pros and cons of vestibular-ocular reflexes

A

It is possible to control eye and head position based on other senses, especially vision but vestibular control is fast and works in the dark

however, anything that disturbs vestibular function, also causes problems with eye position

109
Q

caloric nystagmus

A

Irrigate one ear with water - leads to nystagmus - strong sensationof rotation, nausea

only clinical way to test each ear

mainly effects horizontal semicircular canal (closest to ear)

110
Q

vestibulo-postural reflexes

A

Connections from vestibular nuclei to spinal cord produce postural reflexes in body and neck

these refelxes produce rotation of of head relative to body movements that tend to keep the visual world stationary

ability here varies with species. Owls are very good

linear acceleration contributes to reflexs - cat dropped on back with flip to feet

111
Q

Menier’s syndrome

symptoms

causes

one side

both sides

in children

A

nystagmus, dizziness, nausea, postural problems, deafness and tinnitus (ringing in ear)

caused by genetic mutation, infection, blood supply problems, elevated fluid pressure

Destruction of labyrinth causes extreme nystagmus for several weeks followed by faily complete recovery

loss of both labyrinths causes mild symptoms.

Difference causes the problem, loss isn’t as bad.

children born without vestibular function are pretty normal, but learn to stand and walk more slowly

112
Q

define taste

A

gustation is the sensation evoked by stimulation of taste receptors by water soluble chemicals

113
Q

olfaction

A

is the sensation that results from the detection of odorous substances aerosolized in the environment

114
Q

capsaicin

A

stimulated ion channels in somatosensory nerve fibres, so not a gustatory stimulus.

however, it may stimulate interactions between somatosensory trigeminal nerve fibres in the tongue and taste buds, thus moderating taste

115
Q

different tast sensations

A

umami, salty, butter, sour, sweet

mostly GPCRs

116
Q

tast buds

A

found all over the oral cavity, but most obvious on tongue.

50-100 tase receptor cells in each bud

apical end covered with microvilli that extend into the pore that is open to the external milieu

3-14 afferent nerve fibres per bud. One fibre may innervate more than one bud

taste buds on three types of papillae: cirvumvallate papillae, foliate papillae, fungiform papillae

all taste qualities are detected on all regions of the tongue, though sensitivity to different tasts may vary by region

117
Q

tast receptor cells (4)

A

Type 1 - support cell. Maybe involved in salt taste

Type 2 - releast ATP that acts as NT. Have G protein coupled receptors for bitter, sweet and umami

Type 3 - detect suor taste

B - basal cell

118
Q

Bitter receptors

A

T2R

7 TM domains

detect poison as too bitter

119
Q

sweet receptors

umami receptors

A

2 GPCRs: T1R2 + T1R3

2 GPCRs: T1R1 + T1R3

120
Q

Sour taste transduction

A
  • Protons flow into the taste cells via proton channels
  • depolarization and acidification of the cell
  • Na channels open and K channels close
  • further depolarization
  • Ca influx and GABA + serotonin released

weak (organic) acid are membrane permeable - skip a step but same effects

same cells repond to carbonation

121
Q

salt transduction

A

Na and other cations may be perceived as salty

Low sal concentrations are attractive, high are aversive.

Low salt activates Na ion channels of the ENaC family

Salty tasting ENaC channels are blocked by amiloride in rodesnts, but humans are less sensitive to amiloride

salt transduction can occur at any taste cell

122
Q

Innervation of the esophagus, pharynx and tongue

A

Three cranial nerves:

  • 7 - facial innervates must of fungiform papillae
  • 9 - takes information from back of tongue
  • 10 - vagus, takes info from pharynx
123
Q

adaption in gustatory pathway

A

adaption occurs easily at every step of conduction.

We don’t sense the same chemical for very long

124
Q

Olfaction

olfactory sensory neurons and ORs

A
  • Systen is very sensitive - we can detect about 1 part per billion of methylmercaptan
  • Can discriminate more than a trillion odors
  • Millions of olfactory neurons that are continually replaced by differentiation of stem cells in olfactory mucosa
  • 350-400 different odorant receptor molecule - all GPCRS
  • Each olfactory sensory neuron has one functional OR gene
  • Each OR has detects a small number of odors to a general odor
  • Each olfactory sensory neurons/OR typically respones to a variety of odors so the smell identity is encoded by a combo of OR/OSN responses
  • Women are more sensitive than men
125
Q

Process of olfaction

A
  • Oderant molecule bind to receptors on no-motile cilia
  • Olfactory sensory neurons depolarize and fire APs
  • Sensory info is relayed to glomeruli
  • Information is transmitted to higher regions of the brain
126
Q

olfactory transduction

A

Similar to other G protein signalling cascades

leads to opening of cyclic nucleoside gated channels that are permeable to Ca and Na, leads to depolarization and opening of Ca activated Cl channels

Cl efflux and further depolarization and generation of APs

127
Q

Olfactory bulb

A

Olfactory sensory neurons with the same type of receptor molecule project their acons into the same olfactory glomeruli

They synapse with mitral and tifted cells

Olfactory bulb also recieves input from several CNS areas via centrifugal fibres

Periglomerular interneurons synapse with centrifugal fibres and with mitral and tufted cells. Likely an inhibitory feedback loop

128
Q

neural connections of the olfactory system

A

Olfactory bulb projects directly to olfactory cortex, not via thalamus as other sensory systems do

Olfactory bulb is part of the telencephalon - can be considered the primary olfactory cortex

129
Q

piriform cortex

A

is the largest olfactory cortical area in humas.

activated by all olfactory stimuli but habituates rapidly

130
Q

other olfactory projections

A

parts of amygdala involved. Affective response to smell and alfactory hedonics

hippocampus contributes to learning and behaviour

no known topographical organisation of olfactory bulb onto olfactory cortex

131
Q

anosmia

A

inability to smell

many caues: anatomical, CNA tomour in cribiform plate, olfactory nerve damage

early sign of parkinsins that can precede motor symptoms, and in other neurological diseases too.

olfaction decreases with age

132
Q

hypernosmia

A

enhanced sensitivity to smell - especially in pregnancy

133
Q

olfactory hallucination

A

central origin

Epilepsy, psychiatric aneurism

134
Q

loss of sense of taste

A

caused by smoking, xerostomia, hyperviscosity of saliva, systic fibrosis, brain damage, tumours, drugs

135
Q

carotid body chemoreceptors

A

give information to carotid body and aortic body about chemical composition of blod

innervated by the glossopharynegeal nerve (9)

carotid sinus is a baroceptor

136
Q

alpha rhythms

A

relaxed, awake, eyes closed.

busy wave

137
Q

beta rhythm

A

opening eyes, being alert, even in dark.

Smaller and faster wave

138
Q

structure of a taste bud

A
  1. 50-100 tase receptor cells in each bud
  2. apical end covered with microvilli that extend into the pore that is open to the external milieu
  3. 3-14 afferent nerve fibres per bud. One fibre may innervate more than one bud
  4. taste buds on three types of papillae: cirvumvallate papillae, foliate papillae, fungiform papillae

PHYL 2041 (2 decks)

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