Lecture 8 + Assignment 7 Flashcards

1
Q

Vestibular labyrinth contains 5 things

A

Two otolith organs
- utricle and saccule
= detect head tilt and linear acceleration

Three semicircular canals
- superior, posterior, horizontal
= detect head rotation

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2
Q

Otolith organ orientations

A

utricle
= horizontal hair cells
- face towards striola

saccule
= vertical hair cells
- face away from striola

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3
Q

Otolith organ components

A

otoconia chalk pieces (cal. carbo. CaCO3)
= 1-5 micron diameter

otolithic jelly membrane

hair cells

supporting cells

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4
Q

Otolith organ tilt / lin. acceleration detection

A

otoconia add mass+inertia to the otolithic membrane

makes jelly lag behind

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5
Q

Adaptation of hair cells in otolith organs

A

Transduction:
Head tilt
- more tip link tension
- opens K/Ca channels
- depolarization

adaptation:
- more Ca inside stereocilium
- tip link motor slips
- closes K/Ca channels

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6
Q

3 planes of rotation

A

Yaw
= rotation around z-axis

Pitch
= rotation around y-axis

Roll
= rotation around x-axis
forward and back

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7
Q

Semicircular canal organization

A

are orthogonal to one another (90 degrees)

roughly in the three planes

each detect rotation in their own plane

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8
Q

Semicircular canal components

A

Ampulla: bulge in the bony canal

Cupula: gelatinous substance in which stereocilia are embedded

Crista: epithelial cell layer in which the hair cell bodies are embedded

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9
Q

Semicircular canal detecting acceleration

A
  • cupula displaced in the opposite direction of movement
  • due to endolymph inertia
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10
Q

Rotation stimulus graph

A

transduction (up)

quickly adapts back to the baseline (no more acceleration)

off response (down)
- bumps into cupula from other side when you stop
hair cells hyperpolarize
= firing rate below baseline

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11
Q

Vestibulo-ocular reflex circuitry

A
  • scarpa’s ganglion / cranial nerve 8 comes into the medulla
  • synapses onto neurons in vestibular nucleus
  • decussates in rostral medulla
  • synapses onto abducens nucleus
  • connects to 2 neurons
  • one goes out through 6th cranial nerve
    = releases acetyl choline into muscle (lateral rectus of opposite eye)
  • causes contraction
  • other decussates and ascends into the midbrain
  • release glutamate onto oculomotor nucleus
  • onto 3rd cranial nerve
  • signals to release acetyl choline onto medial rectus
  • causes turn to opposite side
  • both eyes rotate in the opposite direction of head movement
  • inhibitory relaxes the antagonist
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12
Q

Do peripheral nerves decussate

A

no

anything that leaves central does not decussate

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13
Q

3 nerves involved in VOR

A

CN 3 - oculomotor nerve
- motor
- eye movements
- pupil constriction
- upper eyelid muscle

CN 6 - abducens nerve
- abducens or lateral eye movements

CN 8 - vestibulocochlear (auditory) nerve
- hearing, balance

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14
Q

VOR during left rotation

A

activates:
1. the hair cells on the left horizontal semicircular canal
2. the left vestibular nucleus
3. the right abducens nucleus -> right lateral rectus muscle
4. the left abducens nucleus -> left lateral rectus muscle

= rightward eye rotation

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15
Q

Oscillopsia

A
  • bilateral loss of VOR
  • causes thinks to look like they’re shaking + vision blurring
  • can be due to some antibiotics
    ex. hair cells destroyed by ototoxic medications such as streptomycin
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16
Q

Benign paroxysmal positional vertigo (BPPV)

A
  • dislodged otoconia enter posterior semicircular canal
  • causes dizziness in certain head positions
  • can be helped by Epley Maneuver which tries to return them to correct spot
17
Q

Positional alcohol nystagmus

A
  • alcohol enters cupula
  • makes it lighter than endolymph = buoyant
  • causes it to deflect in certain head positions
18
Q

Primary motor and premotor cortex

A

premotor
- in front
- brod. area 6
- lesion here causes apraxia = inability to PLAN and execute complex voluntary motor tasks
- much larger in humans than other animals

primary motor
- further back
- brod. area 4
- correlates to animal size

19
Q

Motor homunculus

A

looks like somatosensory homunculus

  1. corticospinal tract
    - top
    - upper and lower extremities
    - axons go all the way down to the spinal cord
    - cortical efferent
    - commands muscle movements
  2. corticobulbar tract
    - face
    - goes to brain stem motor neurons

cortex layer 5

20
Q

Corticospinal and corticobulbar tracts

A

do this

21
Q

LCST and VCST

A

LCST
- 90% of the CST axons
- decussates in the medulla
- terminates contralaterally in the lateral part of the ventral horn
DISTAL muscles

VCST
- 10% of CST axons
- does not decussate in the medulla
- terminates bilaterally (mainly contralaterally) in the medial ventral horn
AXIAL/PROXIMAL muscles

22
Q

Lateral corticospinal tract topography

A

on the sides of the butterfly

SLTC CTLS

23
Q

Directional tuning of a M1 neuron

A

primary motor complex

  • respond preferentially to a certain angle of movement
  • can do a population vector to see resulting vector
  • ones that fire more have more influence
24
Q

Dr. Apostolos Georgeopolous

A
  • Came up with idea of population vector for the motor cortex
  • M1 neurons basically vote on what to movement to cause
25
Q

Motor neuron pool

A
  • group of alpha motor neurons in the ventral horn of the spinal cord that all go to one muscle
  • can span multiple spinal segments
26
Q

Motor unit

A
  • alpha (lower) motor neuron connects to multiple muscle fibers and causes contraction
  • larger muscles = more fibers innervated by a single alpha motor neuron
  • gives more control and dexterity, more graded movement

ex.
leg muscles = 1000 innervated by 1
fingers = 10
extraocular = 3

27
Q

Neuromuscular junction

A
  • synapse between an alpha motor neuron and a muscle fiber
  • axon releases acetyl choline into a cleft, binds to receptors
  • muscle AP causes contraction

= movement

instead of reuptake, acetylcholine degraded by acetylcholinesterase enzyme

each vesicle = 10 000 ACh molecules
AChE = degrades 5000 molecules/second

28
Q

Amyotropic lateral sclerosis

A
  • Lou Gehrig’s disease
  • death of lower and upper motor neurons
  • flaccid paralysis (loss of muscle tone)
  • muscles atrophy
29
Q

Duchenne muscular dystrophy

A
  • death of skeletal muscles
  • x-linked recessive genetic mutation in gene for dystrophin protein

dystrophin
- helps hold muscle cells together, part of the cytoskeleton

30
Q

Myasthenia Gravis

A
  • autoimmune destruction of skeletal muscle ACh receptors
    = lack of communication
  • alpha motor neurons and muscle NOT damaged
  • normal life expectancy with treatment

ex. inject acetylcholinesterase inhibitor
= keeps ACh in cleft

31
Q

Multi-electrode extracellular recording + Dr. Andrew Schwartz

A

Record from multiple electrodes at the same time
- Very close together on an array

Done by Dr. Andrew Schwartz
- Recordings in monkeys, looked at M1 and resulting arm movement
- M1 population vector just precedes arm movement bc command must travel down
- Could use M1 (brain) to move a robotic arm
Used for human paralysis

32
Q

Inertia

A

an objects resistance to changing speed

due to otoconia or endolymph

33
Q

Shear force direction

A
  • opposite direction of acceleration
34
Q

Muscle spindle

A
  • set of small thin muscle fibers
  • inside main extrafusal fibers, parallel to them
  • 1a afferent axon weaves between them

when the muscle is stretched
- 1a mech gated ion channels open due to deformation
- signals lengthening

35
Q

Golgi tendon organ

A
  • not in parallel to the muscle
    instead in series with it
  • full of collagen fibers and 1b afferent axon weaving between them

when the muscle is stretched
- collagen fibers stretch
- 1b mech gated ion channels open
- collagen hard to stretch = signals tension

36
Q

Gamma motor neuron

A
  • innervates the intrafusal muscle fibers (alpha innervates extrafusal)
  • when muscle contracted and short, slack muscle spindle
  • gamma tightens it up again
  • resets it to detect changes again

makes 1a fire again

37
Q

Knee-jerk / myotatic stretch reflex

A
  • Tap tendon pulls knee down, stretches quadriceps muscle, makes leg kick out
  • Stretch causes contraction
  • Muscles have sensors
  • Upon stretch, mech gated ion channels in muscle spindle cause 1a axons to fire APs
  • Enters dorsal horn, release glutamate onto alpha lower motor neuron = returns to muscle + releases ACh = muscle contraction

Spinal inhibitory interneuron releases GABA onto flexor alpha motor that innervates antagonist muscle

ex.
Head tilting, stretch causes contraction to keep posture

Spring in step be stretch causes contraction again = efficient

38
Q

Autogenic inhibition reflex

A
  • so you don’t hit yourself in the face when lifting a drink

Golgi tendon organ: defects tension in the muscle=APs in 1B axon (btwn tendon/ muscles

Dorsal spinal cord -> ventral horn -> synapse onto inhibitory interneuron -> back to same muscle
REDUCES CONTRACTION

ALSO
- 1B excites excitatory purple interneuron
= activates triceps muscle to oppose movement

39
Q

Flexion-crossed extension reflex

A

Step on something painful
= Adelta or C axon signal

  • Goes to STT AND dorsal horn excitatory interneurons to either excite or inhibit
  • same interneurons decussate

Realises pain
- flexor muscle makes painful foot pull up and relaxes the antagonist muscle

Other side
- opposite
* hamstring relaxed, extensor muscles activated so quad straightens
* you don’t fall over when you put all your weight on one foot

Polysynaptic reflex (multiple synapses)

Polysynaptic excitation of right flexor and left extensor

Polysynaptic inhibition of right extensor and left flexor