MSS: Somatic Nervous System and Muscle Contraction Flashcards
Describe the different types of muscle
Cardiac Muscle
-striated and involuntary muscle in the heart
Skeletal Muscle
- striated and voluntary muscle
- connected to bone and helps in movement
Smooth Muscle
-non-striated and involuntary muscle found in the lining of hollow visceral organs (e.g. digestive tract, respiratory system, blood vessels, bladder) except the heart
Overall Muscle Structure
Muscle Belly Cross-Section
-numerous fasciculi surrounded by perimysium membrane
- each fasciculus contains a bundle of muscle fibres (150 muscle fibres) surrounded by an endomysium membrane
- each muscle fibre in the fasciculi is made of 100-1000s of myofibrils which contain sarcomeres, surrounded by a sarcolemma membrane
Fasciculi
a bundle of muscle fibres (150 muscle fibres)
*each muscle fibre is essentially one cell
100-1000s of myofibrils which contain sarcomeres (contractile units)
Perimycium
Connective tissue that surrounds a fasciculi
Endomysium
The connective tissue surrounding a single muscle fibre in a fasciculi
Sarcolemma
the membrane of myofibrils of skeletal muscle, containing a sarcoplasm surrounding the sarcomeres within the myofibrils
the sarcoplasm contains fat, enzymes, mitochondria, glycogen necessary for muscle function
intertwined between these myofibrils is the sarcoplasmic reticulum where calcium is stored
Myofibrils under a microscope
Contain sarcomeres (contractile units) with areas of dark signal and light signal:
Anisotropic Band (A-band) >high density; contain thick myosin filaments
Isotropic Band (I-band) -light density; contain thin actin filaments
Titin
elastic protein (large molecular spring) attaching myosin to Z band that contributes to elastic recoil of muscle and prevents over-stretching
Sliding Filament Theory
actin filaments slide in between thick myosin filaments to shorten the sarcomere and provide a contraction
ATP facilitates the sliding action
Calcium Stimulated Muscle Contraction
1) Action potential reaches sarcoplasmic reticulum, and calcium released into the sarcoplasm
2) Calcium binds troponin, causing a conformational change in the tropomyosin and exposes the myosin binding sites on the actin
3) Myosin head binds ATP which is hydrolysed by ATPase into ADP and Pi to prime myosin head into a high energy state for binding to myosin binding site on actin filament
4) Using a power stroke, it moves the actin filament towards the centre of the sarcomere for contraction
5) ATP then breaks the bond between actin and myosin head and cycle starts again
Rigor mortis
pumps that pump out calcium fail and there is a massive flood of calcium into the cell, causing muscle fibres to contract, and because there is no ATP being formed, the myosin head remains attached to the actin (sustained contraction) which can last for days
-eventually, the muscle relaxes as the cells break down
Describe the somatic nervous system.
- part of the peripheral nervous system
- provides voluntary control over skeletal muscle.
- The efferent neurons that innervate muscle are called motor neurones.
upper motor neurones from the brain, brainstem and spinal cord synapse with lower motor neurones using glutamate as a neurotransmitter
upper motor neurones from the spinal cord also synapse with individual muscle cells using ACh as the neurotransmitter
Describe the motor unit.
The motor unit is a single motor neurone and all the muscle fibres it controls.
The single fibre contracts completely or not at all.
Motor neurones can innervate a few to a hundred fibres.
How can you regulate the strength of muscle contraction?
by changing the amount of motor units activated
Neuromuscular Junction (NMJ)
point of contact between a lower motor neurone and a skeletal muscle cell
Describe the process of muscle contraction from the neuromuscular junctions.
1) Lower motor neurone synapsed to skeletal muscle and releases acetylcholine (ACh)
2) Action potential moves through the plasma membrane into t tubules
3) Stored calcium released from the sarcoplasmic reticulum into sarcoplasm
4) Calcium binds troponin, causing tropomyosin conformational change revealing the myosin-binding sites
5) Myosin head combines with ATP which is hydrolysed to ADP and Pi, myosin head is cocked/primed and binds myosin-binding sites on actin filament, and moves the actin filament towards the centre of sarcomere for contraction using power stroke
6) Calcium is then pumped out of the cytosol and back into the sarcoplasmic reticulum
7) ATP then breaks the bond between actin and myosin head and cycle starts again
T-tubules (transverse tubules)
invaginations of the sarcolemma which extend excitation deep into the cell where it communicates and interacts with the sarcoplasmic reticulum (calcium store)
Describe cholinergic receptors.
There are two types of cholinergic receptors:
- Muscarinic Receptors (primarily CNS, GPCR, slow)
- Nicotinic Receptors (neuronal/NMJs, fast)
Propagating action potential via nicotinic receptor
2 molecules of Ach bind, resulting in a conformational change in the receptor
ion channel (pore) opens
rapid increase in Na+/Ca2+ and membrane is depolarised leading to muscle contraction
A single action potential will produce a…
single twitch in muscle (lasts 100ms)
-not enough to confer tension to the elastic tendons and bone
Summation
when a second action potential arrives right after the first and before the muscle relaxes, there is the summation of the two, and there is greater tension applied
Tetanus
a continuous contraction that shows no evidence of relaxation
When the rate of action potentials is so high that the muscle doesn’t relax between stimuli, there is a sustained contraction
The fusion of individual twitches generates tetanus
Skeletal muscle tone
Most muscles at rest exhibit some low level of contractile activity
Denervation leads to complete relaxation (flaccid)
Driven by reflex arcs from muscle spindles (sectioning dorsal roots abolishes resting tone)
Describe Duchenne Muscular Dystrophy.
- X-linked degenerative disease
- mutations in gene coding for protein dystrophin
- degradation of structural proteins
- affects both skeletal and cardiac muscle
- unable to walk by 10-12 years; death by 20s due to heart failure
Role of dystrophin protein
connects actin filaments to the sarcolemma/extracellular matrix for mechanical stability and fibre integrity
What does a lack of dystrophin in DMD cause?
dysfunction of sarcolemma stretch, opening ion pores and resulting in an abnormal increase in intracellular Ca2+
Indication of DMD
Due to degradation of structural proteins, creatine kinase (required for ATP) is lost from damaged muscle cells into blood, indicating muscle damage
Describe motor neurone disease.
Motor neurone disease (MND) is a group of disorders that selectively affect motor neurons, the cells that control voluntary muscle activity including speaking, walking and swallowing.
Give some examples of motor neurone disease.
Examples of MNDs are:
- Amyotrophic Lateral Sclerosis (ALS) [affects all motor neurons]
- Progressive Muscular Atrophy [affects only lower motor neurons]
- Primary Lateral Sclerosis [only affects upper motor neurons]
- Progressive Bulbar Palsy [affects motor neurons in the medulla oblongata, involved in swallowing, chewing, etc.]
- Pseudobulbar Palsy [facial muscle movement is affected]
Describe Amyotrophic Lateral Sclerosis (ALS).
- Neurodegenerative disease affecting various motor neurones
- Death usually occurs from respiratory failure within 5 years of diagnosis
- Sporadic probably caused by a combination of environmental and genetic factors- largely unknown
Describe Myasthenia Gravis.
chronic autoimmune neuromuscular disease caused by antibodies attacking ACh receptors at neuromuscular junctions
antibodies block ACh receptor and increase degradation of receptor, causing impaired signal transduction as motor neurones unable to innervate muscle fibres, leading to muscle weakness
affects younger women (20-30) and older men (50-60)
-affects women more 3:2 (F:M)
Treatment of myasthenia gravis
Acetylcholinesterase Inhibitors
-increase ACh at synaptic cleft, more ACh available to innervate muscle
Immunosuppressants
-prevent ACh receptor degradation
*patients live a reasonably normal life and the condition is not life-limiting
