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HYMS Y1 > Block 5 W3 > Flashcards

Block 5 W3 Flashcards

1
Q

What are the 3 types of movements?

A

Reflex
Rhythmic
Voluntary

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2
Q

What are alpha motor neurones?

A

Found in ventral horn of SC.
Thick and myelinated (AP 70-120 m/sec).
Release ACh at terminal.

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3
Q

What is the function of alpha motor neurones?

A

Release of ACh -> contracts muscle fibres for movement.

Lower motor neurones directly activate muscles.

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4
Q

What are the inputs of the alpha motor neurones?

A 
Muscle spindles (Ia afferents - proprioception)
Golgi tendon organs (Ib afferents)
Cutaneous receptors
Spinal interneurones
Upper motor neurones
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5
Q

Define motor neurone disease.

A

Amyotrophic lateral sclerosis (ALS).

Progressive degeneration of alpha motor neurones.

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6
Q

What are the symptoms of ALS?

A

Muscle weakness, atrophy, twitching, abnormal reflexes, difficulty breathing.

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7
Q

What is the treatment of ALS?

A

Riluzole - blocks glutaminergic neurotransmission.

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8
Q

Differentiate between UMN and LMN.

A

UMN - neurones in cerebral cortex and brainstem whose axons remain in CNS and synapses on lower motor neurones directly or indirectly.

LMN - neurones in brainstem and spinal cord whose axons leave the CNS to synapse on muscle fibres. Final coming pathway.

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9
Q

Describe a reflex arc pathway.

A

Stimulus activates sensory receptor, which sends info via afferent sensory neurones to integration centre (CNS), which sends info via efferent motor neurones to the effector organ to perform the response.

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10
Q

Define reflex.

A

Involuntary movement that occurs as a result of sensory stimulation and involves impulses travelling through a reflex arc.
Protects body and coordinates muscle activity.

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11
Q

What does the alpha motor neurones control?

A

Extrafusal muscle.

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12
Q

What does the gamma motor neurones control?

A

Intrafusal muscle.

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13
Q

What is a muscle spindle?

A 
Runs in parallel with muscle
Consist of:
- intrafusal muscle
- Ia sensory neurones
- gamma MN
Stretching causes increase in Ia afferent activity.
For proprioception
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14
Q

What are gamma motor neurones?

A

Maintains tautness of muscle spindle.
Adjusts muscle spindle length to match extrafusal muscle length.
Alpha and gamma - co-activated.

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15
Q

Describe the myotactic reflex.

A

Single synapse between sensory fibre and alpha MN (monosynaptic).
Sensory fibre activation quickly activates the alpha MN, contracting muscle fibres.

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16
Q

Describe the patella tendon tap (knee jerk) reflex.

A

Hammer taps patellar tendon.
Stretches quadriceps muscle and activates Ia afferents.
Impulses travel to SC and activate alpha motor neurones.
Motor neurones release ACh -> contrition of quadriceps = kick.

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17
Q

Describe the reciprocal inhibition in stretch reflex.

A

Patellar tendon reflex involves 2 simultaneous actions:
1. monosynaptic stretch reflex contracts agonist muscle.
2. reciprocal inhibition of the antagonist muscle.
Allows contraction of quadriceps to proceed unopposed so antagonist muscle (hamstrings relax) inhibited via inhibitory interneurone.

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18
Q

Define Golgi tendon organ and its location.

A

Made of collagen and neurones.
Location - junction of muscle and tendon, runs in series with extrafusal muscle.
Innervated by Ib afferents.

19
Q

Why is Ib afferents described as high threshold receptor?

A

Muscle stretch produces little change in neural activity.

20
Q

How does Ib afferents cause muscle contraction?

A

Force generated acts directly on tendon to increase tension of collagen fibrils in Golgi organ -> causes compression of the intertwined sensory receptors and increases Ib afferent activity.

21
Q

What is the function of Golgi tendon organ?

A

Encodes and regulates muscle tension -> prevents muscle overload (if weight too heavy - automatically drop)

22
Q

Describe the inverse stretch reflex.

A

Ib afferents from Golgi tendon organ synapse with inhibitory interneurones in SC.
Activation of Ib decreases activity of alpha MN.
When tension is too much, contraction suddenly ceases and muscle relaxes.

23
Q

Describe the flexor withdrawal/crossed extensor reflex.

A
  1. stepping on pin stimulates nociceptive cutaneous receptors.
  2. signals travel through afferent neurone to interneurones in lumbar SC.
  3. interneurones synapse with alpha MN on both sides.
  4. alpha MN flexes hamstring to bend knee withdrawing stimulated leg.
  5. alpha MN flexes quadriceps on opposite side to extend the leg for compensatory postural support.
24
Q

Define central pattern generator.

A

Neural networks that produce oscillatory (rhythmic) patterned outputs without sensory feedback.
Present in SC and brainstem - consists of local oscillatory circuit of sensory, interneurones and motor neurones.

25
Q

What is the role of CPG?

A

Produces alternating flexion and extension (rhythm) of limbs during locomotion.
Automatic control of rhythmic movements for survival.

26
Q

Why are there cervical and lumbar enlargements?

A

Have large ventral horn, reflecting large number of motor neurones for arms and legs.

27
Q

How are the muscles represented on the spinal cord?

A

Axial -> distal (medial -> lateral)

28
Q

Describe the layers of the muscle.

A

Skeletal muscle (epimysium) -> muscle fascicles (perimysium) -> muscle fibre (endomysium) -> myofibril (sarcoplasmic reticulum) -> sarcomere.

29
Q

What are satellite cells?

A

Precursors to skeletal muscle cells. Quiescent mononucleated myogenic cells.

30
Q

Describe the sarcomere.

A

I-band -> thin actin filaments
A-band -> actin and myosin (dark)
M-line -> connects myosin filament with sarcomere
H-band -> only myosin
Z-line -> separates sarcomere, contains alpha-actin
Titin - anchors myosin to Z-line
Nebulin - determines length

31
Q

Describe the structure of myosin.

A

2 heavy chains and 4 light chains.
Heads - bind actin (cross-bridges).
Hinge.

32
Q

Describe the structure of actin.

A 
Made of troponin and tropomyosin.
Folded in double-strand alpha helix.
Troponin complex:
- TnT binds tropomyosin
- TnC binds Ca2+ ions
- TnI binds actin
33
Q

Describe neuromuscular transmission.

A
  1. depolarisation opens voltage-gated Ca+ channels -> Ca2+ influx -> CaMII binds to synaptic vesicles.
  2. vesicle docks to presynaptic membrane and ACh exocytose.
  3. ACh binds nicotinic ACh receptors on motor end plate.
  4. opens ions channels for Na+ and K+ -> depolarisation/end plate potential.
  5. above threshold, AP triggered.
34
Q

Describe the relaxation of muscle.

A
  • pump Ca2+ out the cell
  • Ca2+ pump sequesters Ca2+ within the SR
  • Ca2+ bound in SR by calreticulin and calsequestrin.
35
Q

Describe excitation-contraction coupling.

A
  1. excitation spreads along the muscle membrane and into transverse tubule invaginations
  2. muscle membrane consists of voltage-activated L-type Ca2+ channels (DHP receptors) arranged in clusters.
  3. clusters are adjacent to Ca2+ channels in SR membrane (ryanodine receptors).
  4. arrival of AP in T-tubule opens DHP receptors and Ca2+ enter the muscle fibre.
  5. Ca2+ entry causes conformational change in ryanodine receptors -> opens and releases Ca2+ into sarcoplasm.
  6. Ca2+ binds troponin C, troponin I moves away from actin and troponin T displaces tropomyosin -> cross-bridge cycling.
36
Q

Describe the cross-bridge cycling.

A
  1. ATP binds myosin head, disengaging from actin.
  2. Hydrolysis of ATP causes change in angle (90) of myosin head.
  3. Head forms cross-bridge with actin two positions along.
  4. Phosphate releases and causes head to change angle (45), filaments slide past each other
  5. ADP is released.
37
Q

Describe the length-tension relationship.

A

At a sarcomere length of about 2.0-2.4µm (which is very close to the resting length in most muscles), the zone of overlap in each sarcomere is optimal, and the muscle fibre can develop maximum tension.

As the sarcomeres are stretched to a longer length, the zone of overlap shortens, and fewer myosin heads can make contact with thin filaments. Therefore, the tension the fibre can produce decreases.

When a skeletal muscle fibre is stretched to 170% of its optimal length, there is no overlap between the thick and thin filaments. Because none of the myosin heads can bind to thin filaments, the muscle fibre cannot contract, and tension is zero.

As sarcomere length becomes increasingly shorter than the optimum, the tension that can develop again decreases. This is because thick filaments crumple as they are compressed by the Z discs, resulting in fewer myosin heads making contact with thin filaments.

Normally the resting muscle fibre length is held very close to the optimum by firm attachments of skeletal muscle to bones (via their tendons) and to other inelastic tissues.

38
Q

What is the role of intramuscular connective tissue framework?

A

Distributes the forces passively imposed on a muscle by stretching.

39
Q

Define rigor mortis.

A

State of muscular rigidity, begins 3-4 hours after death.
Ca2+ diffuse out of SR and allows myosin head to bind actin. No ATP synthesis so cross-bridges form and muscles locked in contraction.

40
Q

Define muscle twitch.

A

Response to stimuli that causes AP in one or more muscle fibres.
3 phases - lag, contraction and relaxation.

41
Q

What is size principle?

A

Low stimulation, small motor neurones controlling small diameter muscle fibres recruited first.
As stimulus increases, larger motor neurones progressively recruited.

42
Q

Define isometric contraction.

A

Muscle develops tension but doesn’t shorten.

43
Q

Define isotonic contraction.

A

Muscle develops tension and causes movement of a load.

HYMS Y1 (25 decks)

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