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Flashcards in Histology of nerve and muscle Deck (12):
1

Describe the basic structure of skeletal muscle

Myofibres arranged in fascicles
Connective tissue
Epimysium
Perimysium
Endomysium
Vascular supply
Innervation
Efferents
Afferents
From spindles
From Golgi tendon organs

2

Skeletal muscle histology

Can be studied by muscle biopsy
Requires the use of frozen sections and good orientation
EM
Molecular tests

3

What is enzyme histochemistry, what does it reveal in skeletal muscle

Enzyme histochemistry reveals different fibre types
-NAPH
-ATPase

4

skeletal muscle fibre types

Slow twitch (red fibres) – type 1, oxidative, fatigue resistant (marathon)
Fast twitch – fatigue rapidly but generate a large peak of muscle tension (sprint)
2A – glycolytic and oxidative (intermediate)
2B – glycolytic (white)

5

What is a motor neuron?

Motor neuron (lower) and the fibres it innervates
-Neuron and its fibres of same type
-Fibre type dependent on neuron
-Size of motor unit varies between muscles

6

How are motor units altered in denervating diseases?

Loss of innervation causes fibre atrophy
Collateral sprouting from adjacent motor units allows reinnervation
Larger motor units result – this can be detected electrophysiologically
Conversion of fibres results in fibre type grouping

7

What occurs in re-innervation?

When muscle fibres have been denervated (they lose their motor neuron)
The fibres can be re-innervated if a different motor neuron innervates them (must be the same type)

8

Describe the organisation of myofibrils

-repeating assemblies of thick and thin filaments
-Thin filaments
a-actin
b-troponin
c-tropomyosin
-Thick filaments
-myosin

9

What occurs during sliding filament theory?

1. Myosin heads bind actin
2. Hydrolysis of ATP provides energy for a conformational change of the myosin head, pulling the actin
3. Sarcomeric shortening due to sliding of the filaments

Accessory proteins
Troponin/tropomyosin – mediate Ca2+ regulation
Maintaining architecture of the filament – e.g. nebulin, titin

10

Sliding filament theory requires ATP - where does this energy come from?

High energy requirement from ATP
Creatine phosphate a short term energy store
CP replenished by creatine kinase (CK)
CK is released on muscle fibre damage
Measurement of serum CK clinically useful

11

What is Dystrophin?

A large protein encoded by a 2.4 million bp gene on Xp21
Confers stability to the muscle cell membrane
Deletion resulting in disruption of the reading frame results in Duchenne
In Becker’s, and in-frame deletion results in a truncated product

12

Describe neuromuscular transmission

1. Nerve impulse results in the release of acetyl choline from synaptic vesicles
2. ACh binds to its receptor
3. Cation entry results in depolarisation, the end-plate potential
4. An action potential travels across the muscle cell membrane and into the T-tubule system
5. Calcium is released from the sarcoplasmic reticulum leading to activation of contraction
6. Dissociated ACh is hydrolysed by acetyl cholinesterase in the NMJ