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Neuromuscular Junction (4 systems involved (Lymphatic/Endocrine (Bacteria…

- - - - Motor neuron fires action potential (AP) down axon
      - Motor neurons axon terminal releases acetylcholine (ACh) into synaptic cleft
    - - The local depolarization triggers an action potential (AP) into adjacent sarcolemma
    - - Action potential in sarcolemma travels down T tubules
      - Sarcoplasmic Reticulum releases Ca2+
      - Ca2+ binds to Troponin, which shifts tropomyosin to uncover myosin-binding sites of actin
      - Myosin heads bind actin
    - - Contraction occurs via cross bridge cycling
      - Neurotransmitters involved in triggering muscle contraction
        
        Acetylcholine
        
        Causes muscles to contract (ACTIVATES MUSCLES)
        
        Activates glandular function in endocrine system
        
        PLAYS IMPORTANT ROLE IN
        
        SIGNAL MUSCLE MOVEMENT
        
        Sensation of pain
        
        Learning and memory formation
        
        Regulation of endocrine system
        
        Regulation of rapid eye movement (REM) cycles
        
        Clostridium Tetani
        
        Toxins Produced
        
        Tetanolysin
        
        2 more items...
        
        Tetanospasmin
        
        4 more items...
        
        What it does at the NMJ
        
        3 more items...
        
        Peripheral Nervous System
        
        ACh is major part of Somatic nervous system
        
        ACh works to activate muscles
        
        Autonomic System
        
        ACh promotes contraction of smooth muscles, dilation of blood vessels, increased body secretions, slower heart rate
  - - - Action Potential arrives at axon terminal of motor neruon
    - - Voltage-gated Ca2+ channels open
      - Ca2+ enter the axon terminal, moving down its electrochemical gradient
    - - Ca2+ entry causes ACh to be released by exocytosis
    - - ACh diffuses across the synaptic cleft and binds to ACh receptors on sarcolemma
    - - ACh binding opens chemically gated ion channels that allow Na+ in and K+ ions out
      - More Na+ ions enter than K+ ions exit, which produces local change in membrane potential called End Plate Potential (EPP)
    - - ACh effects are terminated by its breakdown in the synaptic cleft by acetylcholinesterase and diffusion away from the junction
- - - - Latent Period
        
        Action potential running down sarcolemma, calcium released
        
        Period after stimulus, but before contraction begins
      - Contraction Period
        
        Calcium binds to troponin
        
        begins at power stroke (when myosin pulls actin
        
        Increasing muscle tension
      - Relaxation Period
        
        Calcium pumping out of sarcoplasm and back into sarcoplasmic reticulum
        
        Release of cross bridges
        
        Decreasing muscle tension
- - - - Lock jaw
      - Severe, painful muscle spasms
      - Rigid facial muscles
      - Rigid abdomen, arms, and leg muscles
      - Trouble breathing or swallowing
      - Feeling restless/irritable
      - Fast heartbeat/breathing
      - Headache or seizures
      - Sweating
      - Trouble urinating
      - Low fever
  - - - Due to trouble swallowing or breathing
      - Occurs as result of inhaling the secretions or contents of the stomach
      - Can lead to lower respiratory tract infection
    - - Larynx goes into spasm
      - Prevents oxygen from reaching lungs
      - MAKES BREATHING DIFFICULT
    - - Convulsions
      - Occur in severe cases where tetanus where infection spreads to brain
    - - Caused by blockage in blood vessel
      - Blockage can affect breathing/circulation
    - - The severe spams can cause rhabdomyolysis
      - Rhabdomyolysis
        
        Skeletal muscles are rapidly destroyed, leading to myoglobin to be released into urine
      - CAN LEAD TO ACUTE KIDNEY FAILURE
    - - Repeated spasms can cause fractures in vertebrae and other bones