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Neuromuscular Junction (Tetanus toxins bond to your nerve endings and are…

- - - - Depolarization of terminal membrane causes voltage-gated Ca+ to open
        
        Ca+ enters the cell and triggers the acetylcholine vesicles with the presynaptic membrane
        
        Acetylcholine molecules diffuse across the synaptic cleft and bind to receptor on the postsynaptic membrane
        
        Activated receptors open chemically gated Na+ channels and depolarizes the postsynaptic membrane
        
        Acetylcholine in the synaptic cleft is broken down by the enzyme acetylcholinesterase and the components are taken back up by presynaptic cell for resynthesis
        
        After synaptic transmission, acetylcholine and vesicles are recycled
- - - - Causes local tissue destruction
    - - Causes clinical tetanus
        
        Hypertonicity and generalized severe muscular spasms develop when the tetanus toxin blocks the release of inhibitory neurotransmitters at the NSJ
        
        These spasms often protracted and can cause death by means of severe resistant laryngospasm and respiratory muscle failure
        
        Exocytosis
        
        Cells form a vesicle around material the needs to be expelled from the cell
        
        The vesicles is transported to the cell membrane
        
        The vesicle membrane fuses with the cell membrane and releases the contents from the cell