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Musculoskeletal > Somatic nervous system and muscle contraction > Flashcards

Somatic nervous system and muscle contraction Flashcards

1
Q

Structure of cardiac muscle

A

Straited and lines the wall of the heart, under involuntary control

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2
Q

Structure of smooth muscle

A

Lines visceral organs, spiral structure, under involuntary control

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3
Q

Structure of skeletal muscle

A

Striated and under voluntary control

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4
Q

Muscle structure

A

150 muscle fibres in bundles called fasiculi
The muscle fibre membrane is the sarcolemma and each muscle fibre is made up of 100s-1000s of myofibrils.
Contains the sarcoplasm and the sarcoplasmic reticulum.
Sarcomere

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5
Q

What is the fasiculi?

A

Intricate network of connective tissue, blood vessels etc

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6
Q

What is the function of the sarcoplasm?

A

Required for the correct functioning of the muscle fibre - contains glycogen, fat, enzymes and mitochondria

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7
Q

What is the function of the sarcoplasmic reticulum?

A

Ca2+ release; stores calcium and releases after the stimulation from a motor neuron

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8
Q

What is the sarcomere?

A

It is the contractile unit of muscle

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9
Q

What are the different illuminated structures of the sarcomere?

A
  • Anisotropic band (A-band)
  • Isotropic band
  • Titin
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10
Q

Structure of the anisotropic band

A

High density (thick). Contains the thick filaments made up of predominantly myosin

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11
Q

Structure of the isotropic band

A

Actin filaments - thin filaments made up of predominantly actin

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12
Q

Function of Titin

A

Giant molecular spring - joins the thick filaments to the Z line so when the sarcomere contracts, it passively brings the sarcomere back.

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13
Q

Who theorised the sliding filament model?

A

In the 1950s, Andrew Huxley/Rolf Niedergerke and Hugh Huxley/Jean Hanson

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14
Q

What is the sliding filament model?

A
  • The sarcomere requires ATP for contraction and during contraction, the thick filaments slide between the thin filaments. Actin slides between the myosin. ATP is needed to facilitate the sliding action.
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15
Q

Describe calcium stimulated muscle contraction

A
  1. Motor neuron stimulates the muscle and calcium is released into the muscle cell.
  2. There is a rise in intracellular calcium.
  3. The myosin, which consists of a globular head and a tail, ATP binds to the myosin head where it is hydrolysed.
  4. The breaking of the bond provides energy to help contraction. It releases ADP and inorganic phosphate.
  5. The myosin head becomes cocked and when calcium is present, it enters a high energy state where it binds to actin.
  6. It sits across the actin and causes movement.
  7. ATP is required again for the cycle to occur again. ATP is required to break the actin-myosin bonds.
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16
Q

What happens in rigor mortis?

A

There is no ATP-ADP being formed, so in recently deceased, they are rigid until the proteins are naturally broken down.

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17
Q

How is the myosin head allowed to bind to the action?

A

Troponin forms a complex with tropomyosin and when calcium binds to troponin it causes a conformational change to the troponin. This causes a shift in tropomyosin that uncovers the myosin binding sites on the actin allowing the myosin head to bind to the actin and ratchet along the thin filaments

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18
Q

What is the somatic nervous system?

A

Part of the PNS
Provides voluntary control over skeletal muscle
Efferent neurons that innervate muscle is the motor neurons.
Upper MNs in the brain connect with lower MN in the spinal cord. Signal to muscle.

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19
Q

What is different about the motor neurons compared to other neurons?

A

The neurons in the central nervous don’t leave the brain or spinal cord but the motor neurons do exit via the peripheral nervous system

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20
Q

What is the composition of the motor unit?

A

Single motor neuron and all muscle fibres it controls

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21
Q

What is the all or nothing situation in terms of the single muscle fibre?

A

Single fibre contracts completely or not at all. By innervating multiple muscle fibres, the amount of contraction in a single muscle can be controlled.

22
Q

How can the strength of muscle contraction be regulated?

A

By varying how many activated Motor units there are.

23
Q

What is the neuromuscular junction?

A

The synaptic terminal that receives a stimulus from the brain. This causes the release of an action potential down the motor neuron which causes the release of acetylcholine that is then picked up on the ACh receptors on the synapse causing the membrane to depolarise. The depolarisation moves along the membrane and through the transverse tubules (t-tubules). These enter the muscle and cause depolarisation of the SR that stores calcium. The calcium is then released from the sarcoplasmic reticulum into the cytosol and causes the contraction of the muscle fibres.

24
Q

Describe the action of acetylcholine

A

It is released from the synaptic terminal and binds to its receptors on the membrane. This releases an action potential and depolarises the membrane. This travels down the t-tubules and enters SR and causes the release of stored calcium. The calcium binds to troponin and causes a conformational change. The tropomyosin moves to reveal myosin binding sites on the thin filaments of actin. The myosin head binds to the site and ratchet along the thin filaments. ADP + Pi are recycled to form ATP and allow the cycle to happen again.

25
Q

What are the two types of cholinergic receptors?

A

Muscarinic (primarily CNS, GPCR, slow) and Nicotinic (Neuronal/NMJs, fast)

26
Q

How are the nicotinic AChR activated?

A

2 molecules of Ach bind causing a conformational change in the receptor opening the ion pore. This causes rapid increase in Na2+/Ca2+ and membrane depolarisation leading to muscle contraction.

27
Q

What is a single twitch?

A

A single action potential will produce twitch lasting 100 msec.

28
Q

What causes greater tension?

A

If the 2nd action potential arrives before the muscle gets relaxed there is summation of two.

29
Q

What is tetanus and what does it cause?

A

The rate of action potential so high that the muscle doesn’t relax between stimuli so there is sustained contraction. This causes an increase in fibre tension.

30
Q

What is Duchenne Muscular Dystrophy?

A

Most common severe form of childhood muscular dystrophy.

31
Q

What is the proportion of males that have DMD?

A

1:5000 males

32
Q

What is the pathology behind DMD?

A

There is the mutation in the gene that codes for the protein dystrophin.

33
Q

What does dystrophin do?

A

It is a large protein involved in connecting the sarcomere to the plasma membrane and to the extracellular matrix, required for mechanical stability.

34
Q

What happens if there is a mutation in dystrophin?

A

If there is a mutation in the dystrophin, then the sarcomere don’t attach to the membrane and during contraction, the membrane is torn. It causes the sarcolemma to stretch meaning the ion pores open and increased intracellular calcium. This causes degradation of the muscle fibre.

35
Q

What indicates muscle damage?

A

CK (creatinine kinase) lost from the cell into blood. CK is required for ATP. As a result, this affects skeletal and cardiac muscle.

36
Q

What occurs in people with DMD?

A

Lose ambulation by 10-12 years.

Death by early to mid 20s due to heart failure or CV problems.

37
Q

What is the treatment for DMD?

A
  • Corticosteroids that help to increase ambulation but it isn’t a cure.
  • Drugs that suppress nonsense mutations so there is no mutation in the dystrophin protein.
  • Genome editing has been used to block splicing and cause exon skipping meaning there is a truncated protein missing the mutation from the exon that has been skipped.
38
Q

What are motor neuron diseases (MND)?

A

A group of disorders that selectively affect motor neurons, the cells that control voluntary muscle activity including speaking, walking and swallowing.

39
Q

Name some types of motor neuron diseases

A
  • Amyotrophic Lateral Sclerosis (ALS)
  • Progressive Muscular Atrophy
  • Primary Lateral Sclerosis
  • Progressive Bulbar Palsy
  • Pseudobulbar Palsy
40
Q

What does ALS affect?

A

Affects all motor neurons, in America, it is used as a blanket term for entire spectrum of Motor Neuron Disease

41
Q

What does Progressive Muscular Atrophy affect?

A

Affects lower motor neurons only

42
Q

What does primary lateral sclerosis affect?

A

Affects upper motor neurons

43
Q

What does progressive bulbar palsy affect?

A

Affects motor neurons from the medulla oblongata that is involved in swallowing, chewing etc

44
Q

What does pseudobulbar palsy affect?

A

Affects motor neurons involved in cranial-facial muscle movements

45
Q

What causes death in people with ALS?

A

Ventilatory failure

46
Q

In what number of people is ALS affected?

A

Affects 1:200,000

47
Q

What can cause ALS?

A

5-10% familial through the genes

Sporadic probably caused by a combination of environmental and genetic factors (epigenetic)

48
Q

What are the genes that affect ALS?

A 
30-40% C9orf72
15-20% SOD1
5% TARDBP
5% FUS
These genes are required for normal motor neuron function
49
Q

What is myasthenia gravis?

A

Chronic autoimmune NMD where the body starts producing antibodies against the nicotinic receptors in the NMJ. It results in skeletal muscle weakness and fatigue.

50
Q

How people are affected by Myasthenia Gravis and who is affected?

A

1-7 in 10,000
Young women (20-30 years) and older men (50-60 years)
3:2 (F:M)

51
Q

Describe the mechanisms during myasthenia gravis

A

Body makes antibodies against AchRs at NMJs. It blocks AchRs, increases AchR degradation and causes impaired signal transduction.

52
Q

When is myasthenia gravis worse?

A

It is worse during periods of extended exercise - one of the treatments is to suppress the immune system and prevent Ach receptor degradation. In addition, there is treatments using Acetyl cholinesterase inhibitors.

Musculoskeletal (4 decks)

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