MSS: Somatic Nervous System And Muscle Flashcards
What are the 3 types of muscles and briefly describe them.
- Cardiac muscle - located in the walls of the heart. This is striated and under involuntary control.
- Smooth muscle - located in walls of hollow visceral organs (apart from heart) such as the blood vessels, stomach, digestive tract, bladder, and respiratory tracts etc. They are spindle shaped and under involuntary control.
- Skeletal muscle - muscle attached to skeleton. It is striated and under voluntary control.
Describe the skeletal muscle structure.
- They are formed from a network of muscle tissue, connective tissue, nerves and blood vessels.
- There are various levels of complexity.
- There are up to 150 muscle fibres in bundles called fasciculi. A sheath of connective tissue called the perimycium covers the fasiculi. Myofibres within the fasiculi are also covered by a connective tissue called the endomysium (surrounds each cell).
Each individual muscle fibre (cell) is enveloped by a membrane called the sarcolemma, and they can contain up to 1000 microfibrils which are surrounded by the sarcoplasm.
- The sarcoplasm contains what’s needed for the muscle to function properly: glycogen, fat, enzymes, mitochondria. The sarcoplasmic reticulum is networked though the sarcoplasm as a system of little tubules which surround each myofibril. The SR store Ca2+ and are utilised in calcium release for muscle contraction. Muscle fibrils tend to be multinucleated.
Describe the muscle fibres in skeletal muscle.
Muscle fibres tend to be multinucleated with the nuclei located just under the sarcolemma. Most of the muscle cell is occupied by striated myofibrils.
Muscle function relies on microfilaments, which are actin containing components of the cytoskeleton. Microfilament movement causes contraction. Vertebrate skeleton muscle is attached to the bones and is responsible for their voluntary movement.
Skeletal muscles consist of bundle of long fibres running parallel to the length of the muscle. Each fibre is a single cell with multiple nuclei by the fusion of many embryonic cells.
Myofilaments consist of thick and thin filaments. The thin filaments consist of 2 strands of actin and 1 strand of regulatory protein coiled around each other. The thick filaments are a staggered arrays of myosin molecules.
Each myofibril can be further divided into sarcomeres. Describe them.
The sarcomere is known as the contractile unit. They are repeat subunits which give the characteristic striations and their role is to generate the force that drives movement. It contains an anisotropic band (or A band) which has a high density and is predominantly made up of thick, (myosin) fibres. These have the dark bands.
Titin (a giant protein) joins the thick filaments to the Z line. It acts as a giant molecular spring, so when the sarcomere contracts, it passively brings it back in line.
The thin filaments is made of actin and run parallel to the thick filament and also anchor the z line. Regions of aligned actin filament are known as isotropic (I bands) and are light bands.
The point where adjacent myosin filaments join is called the M line - in the centre of each sarcomere (H zone).
Skeletal muscle is called striated muscle due to the regular arrangement of the light and dark bands.
In a muscle fibre at rest the thick and thin filaments don’t overlap completely.
Describe the sliding filament model.
Explain rigor mortis.
- Actin filaments slide in between thick Myosin filaments.
- The sarcomere requires ATP to facilitate the sliding action
1) Ca2+ ions bind to troponin-C, weakening the bond between troponin and tropomyosin.
2) The troponin molecule changes position, rolling the tropomyosin molecule away from active sites on actin allowing interaction with primed myosin heads (has ATP).
3) The active sites on actin are exposed and myosin heads bind to them, forming cross bridges. ATP is hydrolysed and initially Pi is released for tight binding of actin filament (M head binds to acitn further up).
4) Myosin heads pivot towards the M line, releasing ADP. This action is known as a power stroke. This causes actin to slide along the myosin.
5) Another ATP binds to the myosin heads, breaking the link between myosin and actin. The active site is exposed and able to form another cross bridge. Myosin is now primed again.
6) Myosin reactivates when the free myosin head splits ATP into ADP and a phosphate. The energy released is used to recock the myosin head and the process starts all over again.
If skeletal muscle is deprived of an adequate supply of ATP, then the actin and myosin cannot separate, ATP is required to break acton-myosin bonds.- e.g. Rigor Mortis (Without ATP, myosin molecules adhere to actin filaments and the muscles become rigid).
Summarise the events of the sliding filament theory
The sarcomere is the contractile unit of muscle.
Thick and thin filaments slide passed each other, ratcheting action of Myosin heads (The Sliding Filament Model)
In an un-stimulated muscle: Myosin binding sites (on Actin) are blocked.
Motor neuron stimulation leads to Ca2+ release and binding to Troponin, Tropomyosin conformational change liberates myosin binding sites. Myosin heads attach to binding sites, and power stroke along the Actin. New ATP causes Myosin bridges to detach. ATP re-cocks the Myosin head ready for the next cycle.
By removing myosin, it leaves ghost muscle fibres which fail to respond to ATP. The breakage of one phosphate linkage, provides the energy for the physiological process of muscle contraction.
Muscle stores little ATP so the ADP must be recycled rapidly to ATP. Creatine phosphate is a muscle storage molecule involved in the regeneration of ATP.
Each cycle shorten the sarcomere by 1% (5nm) - hundreds of identical cycles occurring every second results in the muscle contracting very quickly and smoothly. This process requires Ca2+ ions for each actin interaction, and stimulation of neurotransmitter (ACh).
Describe the somatic nervous system.
It is part of the peripheral nervous system. It provides voluntary control over skeletal muscle. The afferent neurones travel to the CNS. The efferent neurones send signals from the CNS to the body via motor neurones.
The upper motor neurones in the brain carry the motor information down the spinal cord to activate the lower motor neurones which then signal to the skeletal muscle causing contraction.
Upper motor neurones work through the neurotransmitter glutamate which transmits the nerve impulses from the upper to the lower motor neurones where its detected by the glutamatergic receptors. The lower motor neurones receive impulses from the upper motor neurones and connect the brainstem and spinal cord to the muscle fibres. They consist of the cranial and spinal nerves.
Describe the motor unit.
In vertebrates each branch motor neuron may form synapses with many skeletal muscle fibres - each fibre however is controlled by a single motor unit.
The motor unit consists of 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.
When a motor neuron produces an action potential, all the muscle fibres in its motor unit contract as a group. The NS can regulate the strength of muscle contraction by varying how many motor units are activated and which units (large or small) are selected.
As more of the neurones controlling the muscle are activated, the process of recruitment increases the force developed by the muscle.
Prolonged muscle contraction = fatigue, depleted stores of ATP + dissipation of ion gradients.
Describe the process of muscle contraction from the neuromuscular junctions.
The action potential arrives at the synaptic terminal of a motor neurone, causing the release of acetylcholine. The Ach binds to its receptors on the muscle fibre, causing it to depolarise the membrane and triggering an action potential in the muscle.
The action potential travels deep into the muscle fibre down the T tubules (infoldings of the plasma membrane) and causes the depolarisation of the sarcoplasmic reticulum, which leads to calcium release from its stores. This calcium is released into the cytosol, which causes the contraction of muscle fibres (through binding to the troponin complex - sliding filament theory).
When the motor neuron input stops the muscle cell relaxes and transport proteins in the SR pump the ca2+ ions out the cytosol. As the ca2+ ion concentration in the cytosol drops the regulatory proteins bound to the thin filaments (troponin and tropomyosin) block the myosin binding sites.
Describe cholinergic receptors.
There are two types of cholinergic receptors:
- Muscarinic Receptors (primarily CNS, GPCR, slow, usually via secondary messenger cascades)
- Nicotinic Receptors (neuronal/neuromuscular junctions, LGICRs, fast, synaptic)
2 molecules of Ach bind to a nicotinic AchR, which causes a conformational change, opening the ion pore.
Consequently there is a rapid increase in Na2+/Ca2+ and the resulting membrane depolarisation of muscle cells leads to muscle contraction.
Describe the graded muscle contractions in skeletal muscle.
A single action potential will produce a twitching that will last for 100 milliseconds; this is known as a single twitch.
If the second action potential arrives before the muscle has relaxed, you get a summation of the two, which leads to greater tension.
When the rate of action potentials is so high that the muscle doesn’t relax between stimuli, the twitches fuse into one smooth sustained contraction known as tetanus (continuous muscle contraction).
Muscle fibres are connected to bones via tendons and connective tissue. Contracting muscle fibre stretches these elastic structures - transmitting tension to the bone.
In a single twitch the muscle fibres starts to relax before connective tissues are fully stretched. During summation
high frequency action potentials maintain an elevated levels of calcium in the cytosol, prolonging the cross bridges cycling and causing greater stretching of the elastic structures.
Describe Duchenne Muscular Dystrophy.
DMD is the most common severe form of childhood muscular dystrophy (1:5000 males from birth). It affects skeletal and cardiac muscle. The patient will be unable to walk by 10-12 years, and death follows by early to mid 20s (usually due to heart failure or respiratory problems).
It’s caused by a mutation in the dystrophin gene. Dystrophin connects actin filaments to the sarcolemma, which is required for mechanical stability.
The lack of dystrophin causes dysfunction of the sarcolemma, causing it to stretch and open the ion pores, increasing the intracellular Ca2+. There is also degradation of structural proteins, and creatine kinase is lost from the cell into the blood (used as a marker indicative of muscle damage). Creatine kinase is required for ATP recycling.
DMD is considered a multi system disease. Patients can experience progress muscle weakness, respiratory insufficiencies, muscular skeletal deformities and cardiomyopathies as well as cognitive impairment, often the autistic spectrum. Progressive pulmonary insufficiencies and orthopaedic issues are a direct results of skeletal muscle weakness whereas the cardiomyopathy and cognitive behavior issues are most likely due to the aberrant dystrophin expression in these tissues.
There is no cure for DMD but there are some treatments. Glucocorticoid steroids (prednisone and deflazacort) can help to improve muscle strength and function. There are also some drugs that can help suppress nonsense mutations.
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]
- Others
Describe Amyotrophic Lateral Sclerosis (ALS).
It’s a neuron disease affecting motor neurons, causing a severe disability that leads to death due to ventilatory failure (lower motor neurones).
It affects 1 in 200,000 individuals. There is a genetic component, with 5-10% being familial.
It’s sporadic, and probably caused by a combination of environmental and genetic factors - though, that is largely unknown.
No diagnostic test available. Brain is unaffected.
- Stephen Hawking was affected by ALS.
