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| The Neuromuscular Junction |
| A normal neuromuscular junction functions as follows: when the terminal neuron fires, it releases acetylcholine into the neuromuscular synapse. The acetylcholine binds to receptors on the surface of the muscle fiber, causing depolarization of the fiber, hence, contracture (Orians, 1983). As one can imagine, this process is key to survival, because it not only explains voluntary muscle movement, but involuntary movement as well (including breathing). |
| Phospholipase A2 |
| Once again, phospholipase A2 is the component in bushmaster venom that disrupts the neuromuscular junction. When it is present (not the natural pancreatic form, but the form found in venom) it competes with acetylcholine for access to receptors on the surface of the muscle (Tu, 1977). When enough of it is present , the muscle fiber becomes uncontractable because all acetylcholine receptors are occupied. Unfortunately for anyone bitten by a bushmaster, the amount of phospholipase A2 in bushmaster venom is about 15 times higher than in its closest relatives. This causes an interesting type of paralysis in which the victim of the bite remains conscious and aware, but has no muscle ability. This is deadly because eventually the diaphragm shuts down, hence respiratory failure. |
