Somatic nervous system and muscle contraction Flashcards

1
Q

What are the 3 vertebral muscle types and describe there structure

A
  1. Skeletal – striated, many nuclei. Uniform cells.
  2. Cardiac – striated, Mononucleate, branched shaped, cells are connected via intercalated discs.
  3. Smooth – non striated, Mononucleate, the actin and myosin interact in a regular way.
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2
Q

Give a brief overview of the structure of the muscle

A
  • Various layers of complexity
  • 150 muscle fibres in bundles: Fasiculi
  • Muscle fibre membrane: sarcolemma
  • Muscle Fibre: 100s- 1000s myofibrils
  • Sarcoplasm: glycogen, fat, enzymes, mitochondria
  • Sarcoplasmic reticulum: Ca2+ release
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3
Q

Describe the structure and organisation of skeletal muscle

A

• Thin filaments align to make up the light band (held together by Z line).
• Sarcomere found between two Z lines → functional unit of the muscle.
• Thin filaments consist of two chains of actin subunits twisted round each other. Tropomyosin wound round actin, attached to globular molecules of troponin. Each troponin complex consists of three polypeptides, one binding to actin, one binding to tropomyosin, one binding to Ca2+ (when available).
At rest, these molecules cover binding sites to which thick filaments can bind.
• Thick filaments consist of bundles of myosin: each myosin has two protruding heads which stick out at each end of the molecule - they are mobile and can bind to thin filaments when binding sites exposed.
• The sliding filament hypothesis - during contraction: light band and H zone get shorter, Z lines move closer and the sarcomere gets shorter (thick and thin filaments slide past one another).

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4
Q

What did the sliding filament theory from 1950 show?

A

Actin filaments slide in between thick Myosin filaments.

• -requires ATP to facilitate the sliding action

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5
Q

How does muscle contract and relax?

A

• Muscle stimulated → action potential passes along sarcolemma down the transverse tubules into the muscle fibre → carried to sarcoplasmic reticulum → calcium ions released into sarcoplasm (from sarcoplasmic reticulum) → calcium ions bind to troponin → alters shape of troponin → pulling the tropomyosin aside → exposes binding sites on actin → ATP hydrolysis occurs, cocking myosin head in position for binding to actin producing ADP and Pi → the myosin head is now in high energy configuration → myosin heads bind to the actin → cross bridges between the filaments form → myosin heads move → actin pulled past myosin filament towards sarcomere, power stroke, ADP is released myosin undergoes a conformational change → ATP binds to myosin causes it to detach, myosin heads detach from actin → ATP is then hydrolysed again so it can bind further up actin filament.
• Once contraction has occurred, calcium ions rapidly pumped back into sarcoplasmic reticulum → relax.
• ATP supplies energy for contraction: ATP attaches to the myosin head → allows movement of myosin.
• Millions of myosin heads are involved in muscle contraction → high demand for ATP.
• Muscle cells only contain enough ATP for 1-2s of contraction, so ATP must be regenerated very quickly:
Aerobic respiration in mitochondria (helped by Bohr effect, limited by rate of oxygen delivery).
Anaerobic respiration in sarcoplasm of muscle tissue (small amounts of ATP, and lactic acid).
Creatine phosphate acts as a reserve store of phosphate groups (added to ADP → ATP)

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6
Q

What is the role of the somatic nervous system?

A
  • Provides voluntary control over skeletal muscle.
  • Efferent neurons that innervate muscle = Motor neurons
  • Upper MNs in brain connect with lower MN in the spinal cord – signal to muscle.
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7
Q

What is a motor unit?

What does it allow?

A
  • Motor unit: single MN and all muscle fibres it controls
  • Single fibre contracts completely or not at all
  • Can regulate strength of muscle contraction by varying how many activated MUs
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8
Q

Describe the structure of a NMJ

A

On image

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9
Q

Describe the cellular events of what happens in a neuromuscular junction

A

On image

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10
Q

What are the 2 types of cholinergic receptors?

A
  • Muscarinic (primarily CNS, GPCR, slow)

* Nicotinic (neuronal /NMJs, Fast)

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11
Q

What happens when Ach bind to a nicotinic receptor?

A

2 molecules of Ach bind to a nicotinin AchR cause conformational change in R = Open ion pore

Consequently: rapid ⬆ Na2+/Ca2+ and membrane depolarisation leading to muscle contraction︎

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12
Q

How do muscles produce graded muscle contractions?

How does it influence the bones?

What causes stretching of the elastic fibres?

A
  • The nervous system can also produce graded whole-muscle contractions by varying the rate of muscle fiber stimulation.
  • A single action potential will produce a twitch lasting for 100 msec or less.
  • If a second action potential arrives before the muscle fiber has completely relaxed, the two twitches sum, resulting in greater tension.
  • Further summation occurs as the rate of stimulation increases.
  • When the rate is so high that the muscle fiber cannot relax between stimuli, the twitches fuse into one smooth, sustained contraction called tetanus.
  • Because muscle fibers are connected to bones via tendons and connective tissues, a contracting muscle fiber stretches these elastic structures, transmitting tension to the bones.
  • In a single twitch, a muscle fiber begins to relax before connective tissues are fully stretched.
  • During summation, high-frequency action potentials maintain an elevated concentration of calcium in the cytosol of the muscle fiber, prolonging cross-bridge cycling and causing greater stretching of the elastic structures.
  • During tetanus, the elastic structures are fully stretched, and all of the tension generated by the muscle fiber is transmitted to the bones.
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13
Q

What is Duchenne Muscular Dystrophy?

A
  • DMD most common severe form of childhood muscular dystrophy (1:5000 males). Mutated gene: Dystrophin
  • Skeletal + cardiac
  • Unable to walk by 10- 12 yrs, Death by early to mid 20s (heart failure)
  • Connects actin filaments to the sarcolemma, required for mechanical stability
  • Lack of dystrophin causes dysfunction of sarcolemma stretch = ion pores open and increased intracellular Ca2+.
  • Degradation of structural proteins, CK lost from the cell into blood (indication of muscle damage). CK required for ATP.
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14
Q

What is motor neurone disease?

A

Motor neuron disease (MND) is a group of disorders that selectively affect motor neurons, the cells that control voluntary muscle activity including speaking, walking and swallowing.

On image

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15
Q

What is Amyotrophic lateral sclerosis (ALS)?

A
•	ND disease affecting MNs, severe disability leading to death from respiratory failure (Lower MNs).
•	Affects 1:200,000
•	% familial
o	-30-40% C9orf72
o	-15-20% SOD1
o	-5% TARDBP
o	-5% FUS
•	Sporadic probably caused by a combination of environmental and genetic factors – largely unknown!
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16
Q

What is Myasthenia Gravis?

A
  • Chronic autoimmune NMD results in skeletal muscle weakness and fatigue.
  • 1-7 in 10,000
  • Young women (20-30 yrs) and older men (50-60 yrs)
  • -3:2 (F:M)
  • Body makes antibodies against AchRs at NMJs
  • Blocks AchRs, increases AchR degradation and causes impaired signal transduction