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Neuromuscular Junction (NMJ) (Background (chain of events at neuromuscular…
Neuromuscular Junction (NMJ)
Background
systems involved :
Nervous System
tetanus toxin is a neurotoxin
transported in the axons
affects four different areas of the nervous system
blocks the release of other neurotransmitters
Lymphatic System
the tetanus toxin is transported with lymph vessels
Muscular System
neurotoxin is taken up by endocytosis at the neuromuscular junctions
end result is muscles in fused tetanus
muscle spasms
Cardiovascular System
the tetanus toxin is transported with lymph vessels
chain of events at neuromuscular junction
an action potential is sent down the axon of a neuron which opens the voltage gated Ca2+ channels
the synaptic vesicles release a hormone called ACh or acetyl colene by exocytosis because of Ca2+ entering the axon terminal
ACh is a neurotransmitter, it enters the synaptic cleft where it binds to the ACh receptors
ACh's binding opens chemically gated ion channels (Na K pump) +more sodium enters then potassium exits which changes the membrane potential = end plate potential =local depolarization
this depolarization causes an AP down the rest of the sarcolemma as ion channels further along are opened
The AP reaches the t tubules and cisterns which have voltage sensitive proteins on them
the proteins change shape and release Ca2+ from the cisterns into the cytosol
muscle contraction begins
this opens the active sites on actin and myosin forms cross bridges
contraction occurs
Ca2+ binds to troponin which moves tropomyosin
neurotransmitters for muscle contraction
ACh, acetyl colene
receptors open chemically gated ion channels which starts an action potential that leads to muscle contractions
binds to ACh receptors
ACh is released by synaptic vesicles in the axon terminals
GABA
principal inhibitory neurotransmitter of the brain
substances that block its release induce convulsions
glycine
principal inhibitory neurotransmitter of the spinal cord
blockage results in uncontrolled convulsions and respiratory arrest
exocytosis steps
Proteins at the vesicle surface (v-snares) bind with t-snares (plasma membrane proteins).
The vesicle and plasma membrane fuse and a pore opens up
Membrane bound vesicle migrates to the plasma membrane
Vesicle contents are released to the cell exterior
Contractility
summation
occurs when the second contraction begins before the muscle is completely relaxed
contractions are added together
Temporal Summation
Tetanus
as wave summation increases 2 things can occur
Fused Tetanus
maximal tension
all evidence of muscle relaxation dissapears
contractions fuse into a smooth sustained contraction
Unfused Tetanus
sustained quivering contraction
Ca2+ concentration in cytosol rises continuously
relaxation time between twitches becomes shorter and shorter
twitch
the response of a muscle to a single stimulation
fibers contract quickly and then relax
myogram
recording of contractile activity consisting of one or more lines of tracings
show the amount of tension a muscle develops when its length is held constant as it contracts
Twitch Myogram
Period of Relaxation
10-100ms contractile force is declining, muscle tension decreases to 0
Period of Contraction
Cross Bridges are active from onset to peak tension development. 10-100ms
Latent Period
excitation-contraction coupling is occurring but the muscle tension is not measurable
Clostridium Tetani
spore-forming bacterium, neurotoxin
spores are often found in dust, soil, and animal feces
transmitted through contaminated puncture wounds, fractures, unclean or hygenic work care practices, animal feces
not communicable person to person
resistant to boiling and freezing
remain viable for years
tetanus occurs when the spores of c. tetani are in oxygen heavy wound environments
germinate and produce a neurotoxin
tetanus toxin is very potent, transported with blood and lymph vessels
taken up by endocytosis at the neruomuscular junctions
transported centripetally inside the axons
tetanus toxin acts on four areas of the nervous system
spinal cord
the brain
motor end plates
sympathetic system
tetanus toxin blocks the release of glycin and GABA in the CNS
glycine and GABA are inhibitory neurotransmitters
without the inhibitors the excitatory nerve impulses are unopposed resulting in muscle spasms
Downstream
indirect
patient went to hosptial after serious disease progression
patient ignored symptoms until he couldnt speak and was having severe spasms
patient never recieved vaccinations
no built up immunity
tattoo artist used dirty needles
caused a puncture wound
puncture wound became infected with tetanus spores because of lack of work care hygeine
direct
Why Spasms?
the toxin blocks the release of inhibitory neurotransmitters
the excitatory responses build up and have nothing to stop them
flaccid paralysis wouldnt be possible
blockage of glycine and GABA results in muscle spasms
Upstream
Toxin Side Effects
fever
sweating
fast heart rate
abnormal heart rhythm
high blood pressure
difficulty swallowing
brain damage due to lack of oxygen
muscle spasms and stiffness in various muscles
bone fractures of spine due to convulsions
Untreated :
without treatment tetanus can be fatal
aspiration pneumonia
laryngospasm
fractures
tetanic seizures
pulmonary embolism
severe kidney failure
11% of reported cases of tetanus are fatal
patients often suffocate because the toxin's effect on respiratory muscles can interfere with breathing
