Neuromuscular JUNC

Question 1

Mechanism of excitation contraction in skeletal muscles

Answer 1

1, influx of Ca2+ to presynapse 2, release of neurotransmitter 3, binding of ACh to nicotinic receptors 4, influx of Na+ at motor end 5, propagation of AP 6, activation of T-tubules DHPR 7, release of calcium from SR 8, binding of ca to troponin 9, cross bridge formation with actin and myosin 10, power stroke and release of ADP + Pi

Question 2

Role of Ca2+

Answer 2

Calcium released from terminal cisternae of SR
Contractile machinery activated
Ca2+ pumped back into SR via longitudinal tubules (requires ATP)
Ca2+ diffuses back into terminal cisterae to be released again

Question 3

ATP generation in skeletal muscles

Answer 3

Dephosphorylation of phosphocreatine 
ADP+PC—->ATP+C (Lohmann reaction)
Glycolysis 
Glycogen+2ATP—->Lactic acid + 4ATP (Accumulates H+)
Oxidation of glucose
Glucose+2ATP—OXYGEN->6O2+6H2O+ nATP
Oxidation of FFA
FFA—O2—>CO2+H2O+nATP (HIGH YEILD)

Question 4

Titanic fusion frequency

Answer 4

Twitch- muscles can relax between stimuli
Tetanic- stimuli are frequent so contraction in maintained
Single twitch, Temporal, Unfused and Fused
TFF can vary with differing muscles and temp

Question 5

NMJ adaptation to training

Answer 5

• greater efficiency in recruitment patterns
• increased motor excitability
• increased CNS activation

Question 6

Two fundamental adaptations of muscle fibres

Answer 6

• increase protein synth
• proliferation of satellite cells
• microfibrils thicken and increase

Question 7

Muscle fibre remodelling

Answer 7

Fusion of satellite nuclei and incorporate into existing muscle cells allow them to synthesise more protein

Question 8

Neurogenic disorders- POLIOMYELITIS

Answer 8

Destruction of motor neurone cell bodies
Impairment of both voluntary and reflex action
Muscular atrophy

Question 9

NMJ disorders- Lambert Eaton syndrome

Answer 9

Defective ACh release
Metabolic endocrine myopathies
-high circulating corticosteroids or thyroid in blood

Question 10

Genetic Myopathies

Answer 10

Muscular dystrophies-muscle destruct
Metabolic-defective enzymes
Myotonias-sustained contract with slow relax
Channel proteins-impaired function of ion channels

Question 11

Duchenne Muscular Dystrophies

Answer 11

Dystrophin on X chromosomes 
When dystrophin is absent 
-membranes become leaky to Ca2+ 
-proteolytic enzymes become activated 
-Contractile machinery are destroyed

Question 12

Upper motor neurone lesions

Answer 12

Impairment of voluntary activity and spinal reflexes often are exaggerated
No muscle atrophy

Question 13

Lower motor neurone lesions

Answer 13

Impairment of both voluntary and reflex activity

Muscle atrophy

Question 14

Mutation of CLC-1 gene

Answer 14

Myotonic Congenita 
Auto Dom Thomsen type
Auto Ress Becker type
“Channelopathies”
-gating function may be impaired

Question 15

K+ accumulation

Answer 15

Normal muscle has high CLC-1 and its conductance counteracts the depolarising effect of K+ accumulation I the T-tubules

Question 16

Myotonia

Answer 16

Deceased function of CLC-1 = small accumulation of K+ will cause membrane depolarisation

Question 17

CLC-1

Answer 17

80% of resting membrane potential conductance in smooth muscle
It’s decrease increases excitability so single nerve can trigger chain of AP

Question 18

Treatment for myotonia

Answer 18

Inhibit voltage gated channels = decreased excitability

Warm up exercises to relieve stiff muscles

Question 19

Periodic paralysis

Answer 19

Rare autosomal dominant disorder associated with mutations of sodium potassium and calcium channels
Muscle weakness