NMJ, muscle contraction

Question 1

NMJ is between?

Answer 1

between a motor neuron and a muscle fibre

Question 2

NMJ label
(slide 4, lecture 5)
Main structures

Answer 2

Main structures
presynaptic nerve terminal
synaptic cleft
postsynaptic endplate region on the muscle fibre

Question 3

Allows for?

Answer 3

unidirectional chemical communication between peripheral nerve and muscle

Question 4

Acetylcholine role?

Answer 4

NT for voluntary striated muscle

Question 5

single muscle fibre will have innervation from

Answer 5

a branch of a SINGLE MOTOR neurone only
(not both afferent/ efferent)
In injury this isn’t the case so can differentiate between injured muscle

Question 6

Types of motor neurones

Answer 6

Upper (brain)

Lower (brainstem+ spinal cored)

Question 7

Afferent neurones bring information into cord through

Answer 7

Dorsal route (dorsal ganglion)

Question 8

Efferent neurones take information out of cord in

Answer 8

anterior horn (grey body of spinal cord)

Question 9

Process when action potential reaches NMJ

Answer 9

1. Action potential open V-gated Ca2+ channels
2. Ca2+ enters
3. Ca2+ triggers exocytosis of vesicles
4. Acetylcholine diffuses in cleft
5. Acetylcholine binds to receptor-cation channel & opens channel
6. Local currents flow from depolarized region and adjacent region; action potential triggered and spreads along surface membrane
7. Acetylcholine broken down by acetylcholine esterase (enzyme). Muscle fibre response to that molecule of Acetylcholine ceases

Question 10

Normal physiology of NMJ

Answer 10

Individual vesicles release ACh at a very low rate causing miniature end-plate potentials (MEPPs)

Question 11

Skeletal muscle structure

slide 10, lecture 5

Answer 11

-

Question 12

Myofibres- composition
Covered by?
Cytoplasm=?
Composed of?

Answer 12

Covered by plasma membrane – sarcolemma
T-tubules tunnel into centre
Cytoplasm called sarcoplasm – myoglobin and mitochondria present
Network of fluid filled tubules – sarcoplasmic reticulum
Composed of myofibrils

Question 13

Myofibrils
Diameter
Composed of?

Answer 13

1-2μm in diameter
Extend along entire length of myofibres
Composed of two main types of protein – actin and myosin

Question 14

Myofilaments

Answer 14

Light and dark bands give muscle striated appearance
Do not extend along length of myofibers
Overlap and are arranged in compartments called sarcomeres

Question 15

Cnocentric contraction

Answer 15

muscle gets shorter

Question 16

Eccentric contraction

Answer 16

muscle gets longer

Question 17

Myofilaments

Answer 17

Dense protein Z-discs separate sarcomeres
Dark bands – A band (thick - myosin)
Light bands – I band (thin - actin)
Myosin and actin filaments overlap

Question 18

Sliding filament theory changes in bands

Answer 18

I band became shorter
A-band remained same length
H-zone narrowed or disappeared

Question 19

Muscle activation process

Answer 19

1. Action potential propagates along surface membrane and into T-tubules
2. DHP (dihydropyridine) receptor in T-tubule membrane: senses ΔV & changes shape of the protein link to Ryanodine receptor, opens the Ryanodine receptor Ca2+ channel in the SR membrane; Ca2+ released from SR into space around the filaments
3. Ca2+ binds to Troponin & Tropomyosin moves allowing
4. Crossbridges to attach to actin
5. Ca2+ is actively transported into the SR continuously while action potentials continue. ATP- driven pump (uptake rate < or = release rate).
6. Ca2+ dissociates from TN when free Ca2+ declines; TM block prevents new crossbridge attachment; Active force declines due to net crossbridge detachment

Question 20

Disorders of NMJ

Answer 20

Botulism
Botulinum toxin produces an irreversible disruption in stimulation-induced acetylcholine release by the presynaptic nerve terminal
Stops the release of acetylcholine into the synaptic cleft

Myastenia gravis (MG)
An autoimmune disorder where antibodies are directed against the acetylcholine receptor (Acetylcholine gets to the receptor but the receptor doesn’t bind to it (binds to antibody instead)

Lambert-Eaton myastenic syndrome (LEMS)
an autoimmune disease caused by antibodies directed against the voltage-gated calcium channel (VGCC) - associated with lung cancer.
Muscle doesn’t contract because action potential arrives to muscle but Ca Induced Ca Release