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Man gets a tattoo from sketchy tattoo artist then experiences spasms and…
Man gets a tattoo from sketchy tattoo artist then experiences spasms and has difficulty talking
what is neuromuscular junction?
is the region where the motor neuron contacts the skeletal muscle
when axons travel from central nervous system to the skeletal muscle
each axon divides into many branches as it enters the muscle
when axons branches on the end of the muscular fiber it forms a neuromuscular function (NMJ)
every muscle fiber has one neuromuscular junction with one motor neuron
axon- long threadlike extensions of motor neurons
neuromuscular junction anatomy
consist of axon terminal, synaptic cleft, and motor end plate
axon terminal and muscle fibers are separated by a Gell-filled space called a synaptic cleft
stored within axon terminals are membrane-bound synaptic vessels
synaptic vesicles contain neurotransmitter acetylcholine
axon terminal- end of an axon
motor end plate- oval shaped and highly excitable region of sarcolemma in closest proximity to the axon terminal
where sarcolemma is folded, called junctional folds, contains millions of ACh receptors
The big picture
Four steps that must occur for the skeletal muscle to contract
Events at neuromuscular junction
AP arrives at axon terminal
Voltage-gated calcium channels open and calcium enters motor neuron
Calcium entry causes release of ACh neurotransmitters into synaptic cleft
ACh diffuses across to ACh receptors on sarcolemma
Na+chemical gates
muscle fiber excitation
Action potential goes along motor neuron to axon terminals
voltage gated calcium opens, calcium ion diffuses along terminal
because calcium enters it causes synaptic vessels to release ACh via exocytosis
ACh diffuses along synaptic cleft , binds to ACh receptors contain ligand gated cation channels
ligand gated cation channels open
sodium ions enter muscle fiber sodium ions exit muscle fiber causes membrane potential to be less negative
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excitation-contraction coupling
events that transmit AP along sarcolemma (excitation) are coupled to sliding of myofilaments (contraction)
AP is propagated along sarcolemma and down into T-tubules, where voltage-sensitive proteins in tubules stimulate Ca2+ release from SR
Ca2+ release leads to contraction
cross bridge cycling
at low intracellular Ca2+ concentration
Tropomyosin blocks active sites on actin
Myosin heads cannot attach to actin
Muscle fiber remains relaxed
Voltage-sensitive proteins in T tubules change shape, causing sarcoplasmic reticulum (SR) to release Ca2+ to cytosol
At higher intracellular Ca2+ concentrations, Ca2+ binds to troponin
Troponin changes shape and moves tropomyosin away from myosin-binding sites
Myosin head is then allowed to bind actin, forming cross bridge
cycling is initiated, causing sarcomere shortening and muscle contraction
when nervous stimulation ceases Ca2+ is pumped back into SR, and contraction ends
Four steps of the cross bridge cycle
cross bridge formation
High-energy myosin head attaches to actin thin filament active site working (power) stroke
Myosin myosin head pivots and pull thin filament toward M line
cross bridge detachment
ATP attaches to myosin head
This causes cross bridge to detach
cocking of myosin head
Energy from hydrolysis of ATP "cocks" myosin head into high-energy state
This energy will be used for power stroke in next cross bridge cycle
Generation of an AP across the Sarcolemma
occurs in three steps
Generation of end plate potential
ACh releases from motor neuron to ACh receptors on sarcolemma
Causes chemically gated ion channels (ligands) on sarcolemma to open
Na+ diffuses into muscle fiber
Because Na+ diffuses in, the interior becomes less negative (more positive)
Results in local depolarization called end plate potential
Some K+ diffuses outward, but not much
Depolarization
Generation and propagation of an action potential (AP)
If end plate potential causes enough change in membrane voltage to reach critical level called threshold, voltage-gated Na+ channels in membrane will open
Large influx of Na+ through channels into cell triggers AP that is unstoppable and will leaf to muscle fiber contraction
Ap spreads across sarcolemma from one voltage-gated Na+ channel to the next one in adjacent ares, causing that area to depolarize
Repolarization
restoration of resting conditions
Na+ voltage-gated channels close, and voltage-gated K+ channels open
K+ effluxes out of cell rapidly bringing cell back to initial resting membrane voltage
Refractory period- muscle fiber cannot be stimulated for a specific amount of time, until depolarization is complete
iconic conditions of resting state are restored by Na+-K+ pump
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resting sarcolemma is polarized
action potential is caused by electrical charges
polarized- voltage exists across membrane inside of cell is negative compared to outside
Muscle contraction
contraction produces muscle tension, the force exerted on load or object to be moved
contraction may or may not shorten muscle
Isometric contraction
no shortening; muscle tension increases but does not exceed load
Isotonic contraction
muscle shortens because muscle tension exceeds load
force and duration of contraction vary in response to stimuli of different frequencies and intensities
each muscle is served by at least one motor nerve
Motor nerve contains axons of up to hundreds of motor neurons
Axons branch into terminals, each of which forms NMJ with a single muscle fiber
motor unit is the nerve-muscle functional unit
motor unit consist of the motor neuron and all muscle fibers it supplies
number of muscle fibers can vary from a few to several hundred
smaller the fiber number, the greater the fine control
muscle fibers from a motor unit are spread throughout the whole muscle, so stimulation of a single motor unit causes only weak contraction of the entire muscle
Muscle twitch
the simplest contraction resulting from a muscle fiber's response to a single action potential from a motor neuron
twitch can be observed and recorded as a myogram
There are three phases of a muscle twitch
period of contraction
cross bridge formation
tension increases
period of relaxation
Ca2+ reentry into SR
tension declines to zero
latent period
events of excitation-contraction coupling
no muscle tension seen
muscle contracts faster than it relaxes
Differences in strength and duration of twitches are due to variations in metabolic properties and enzymes between muscles
ex: eye muscles contraction are rapid and brief, where as larger, fleshy muscles (calf muscles) contract more slowly and hold it together
Graded muscle responses
Normal muscle contraction is relatively smooth, and strength varies with needs
graded muscle responses vary strength of contraction for different demands
Responses are graded by
Changing frequency of stimulation
The higher the frequency, the greater the strength of contraction
Changing strength of stimulation
The stronger the stimulation, the more motor units are activated, and the stronger the contraction
required for proper control for skeletal movement
a muscle twitch is only seen in a lab setting or with neuromuscular problems, but not in a normal muscle
In the body, the brain determines the strength of a muscles contraction by changing
The rate of firing of action potentials along the axon of its motor neuron (frequency)
The number of its motor neurons that new activated (strength)
Muscle responds to changes in stimulus frequency
Single stimulus results in single contractile response (muscle twitch)
wave temporal summation results if two stimuli are received by a muscle in rapid succession
If stimuli frequency increases, muscle tension reaches near maximum
If stimuli frequency further increase, muscle tension reaches maximum
referred as fused (complete) tetanus because contractions "fuse" into one smooth sustained plateau
Prolonged muscle contractions lead to muscle fatigue
produces smooth, continuous contractions that add up (summation)
Further increase in stimulus frequency causes muscle to progress to sustained, quivering contraction referred to as unfused (incomplete) tetanus
muscle fibers do not have time to completely relax between stimuli, so twitches increase in force with each stimulus
Additional Ca2+ that is released with second stimulus stimulates more shortening
Muscle response to changes in stimulus strength
Recruitment- multiple motor unit summation
Types of stimulus involved in recruitment
Threshold stimulus
Stimulus is strong enough to cause first observable contraction
Maximal stimulus
Strongest stimulus that increases maximum contractile force. All motor units have been recruited
Subthreshold stimulus
stimulus not strong enough, so no contraction seen
Muscle works on size principle
motor units with smallest muscle fibers are recruited first
motor units with larger and larger fibers new recruited as stimulus intensity
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stimulus is sent to more muscle fibers, leading to more precise control
Isotonic contractions
muscle changes in length and moves load
isotonic contractions can either be concentric or eccentric
concentric contractions
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eccentric contractions
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isometric contractions
load is greater than the maximum tension muscle can generate, so the muscle neither shortens or lengthens
ex: pushing a wall
electrochemical and mechanical events new same in isotonic or isometric contractions, but results are different
ATP
ATP supplies the energy needed for the muscle fiber to
pump calcium back into SR
pump Na+ out of and K+ back into cell after excitation-contraction coupling
move and detach cross bridges
Available stores of ATP depleted in 4-6 seconds
ATP is the only source of energy for contractile activities: therefore it must be regenerated quickly
ATP is generated quickly by three mechanisms
Anaerobic pathway: glycolysis and lactic acid formation
ATP can also be generated by breaking down using energy stored in glucose
Glycolysis- first step in glucose breakdown
does not require oxygen
Glucose is broken into 2 pyretic acid molecules
2 ATP are generated for each glucose broken down
Low oxygen levels prevent pyruvic acid from entering aerobic respiration phase
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Aerobic pathway
Produces 95% of ATP during rest and light to moderate exercise
Consist of chemical reactions tat occur in mitochondria and require oxygen
fuels used glucose from glycogen stored in muscle fiber, then blood glucose, and free fatty acids
Fatty acids are main fuel after 30 minutes of exercise
Breaks glucose into CO2, H2O and large amount of ATP (32 can be produced)
Slower than anaerobic pathway
Direct Phosphorylation of ADP by
creatine phosphate
(CP)
Creatine phosphate is a unique molecule located in muscle fibers that donates a phosphate to ADP to instantly form ATP
Muscle fibers have enough ATP and CP reserves to power cell for about 15 seconds
Clostridium Tetani
form of spastic paralysis caused by toxin produced by Clostridium tetani
Penetrating wound with soil prone to developing C retain infection
Blocks release of inhibitory neurotransmitters in spinal cord
results in overstimulation of muscles
routine vaccination against this life-threatening condition
progresses to fixed fidgety of the jaw (lockjaw) and trunk/limb muscle spasms
usually fatal due to respiratory failure
how clostridium tetani affect the patient
muscular system
respiratory system
nervous system
integumentary system
Exocytosis
transport out of cell
Usually activated by cell-surface signals or changes in membrane voltage
Process where large substance is ejected from cell
Substance being ejected is enclosed in secretory vesicle
Some substances exocytosed: hormones, neurotransmitters, mucus, cellular wastes
If the toxin remains in the patient’s bloodstream, what other effects might the toxin have?
death
Blocks release of inhibitory neurotransmitter in spinal cord
Why is it deadly untreated?
causes respiratory failure
form of spastic paralysis
why
Results in overstimulation of muscles
The patient got a tattoo from a "sketchy" tattoo artist
the needle was dirty that why he was diagnosed with Clostridium tetani
toxin was on the needle that penetrated his skin