Sandbox Reserved 1453

This Sandbox is Reserved from Jan 22 through May 22, 2018 for use in the course Biochemistry II taught by Jason Telford at the Maryville University, St. Louis, Missouri, USA. This reservation includes Sandbox Reserved 1446 through Sandbox Reserved 1455.

To get started: Click the edit this page tab at the top. Save the page after each step, then edit it again. Click the 3D button (when editing, above the wikitext box) to insert Jmol. show the Scene authoring tools, create a molecular scene, and save it. Copy the green link into the page. Add a description of your scene. Use the buttons above the wikitext box for bold, italics, links, headlines, etc. More help: Help:Editing

Acetylcholine receptor and its reaction to cobra venom

spinqualitylabelsall models Caption for this structure Show:Asymmetric Unit Biological Assembly Drag the structure with the mouse to rotate   Export Animated Image   Print3D This is a default text for your page '. Click above on edit this page' to modify. Be careful with the < and > signs. You may include any references to papers as in: the use of JSmol in Proteopedia or to the article describing Jmol to the rescue. Structure The acetylcholine receptor is composed of five alpha helical chains each with about 370 amino acids. This is a transmembrane protein forming a funnel into the cytosol of the cell. Alpha and beta receptors Acetylcholine Function as a Signal Molecule Receptor The neurotransmitter acetylcholine is released into the synaptic cleft and is bound to the acetylcholine receptor. Consequently, the receptor changes conformation to release potassium ions into the cytoplasm of the cell while sodium ions are ejected from the cell through the receptor acting as an ion-gated channel. This change in ion concentration causes a change in the membrane potential of the cell. The release of sodium into extracellular matrix causes a release of more acetylcholine in a neighboring cell continuing the action potential across nerve cells. Nerve cell communication is also in control of muscle contraction. When the action potential traveling down the nerve cell reaches muscle tissue, the muscle cell responds by triggering a release in calcium to allow for muscle contraction for the organism to move. Cobra Toxin Cobra venom has several detrimental effects on their prey. This toxin blocks the acetylcholine receptor which causes paralysis of the muscles, including the diaphragm which leads to asphyxiation. Only about 1/3 of the acetylcholine receptors need to be blocked to cease function of the diaphragm resulting in death in as little as thirty minutes. Cobra Venom Cobra Toxin interaction with Acetylcholine When cobra venom is introduced into the body is moves along the bloodstream to a diaphragm muscle. It works as a postsynaptic neurotoxin by interacting with OH group leaving the acetyl choline channel open which releases ions used in creating an action potential. Without the ions the diaphragm muscle can not be activated to contract and will not move so an individual can not take a breath. Anti-Venom There are only two ways to save a life after being infected with cobra venom the first being an artificial respirator to contract and expand the lungs until the diaphragm is able to start an action potential and contract on its own. The other option to a quick administration of an anti-venom. Anti-venom acts to bind the venom both in the receptor and in the bloodstream and allows for it to be excreted out of the body. This is a sample scene created with SAT to color by Group, and another to make a transparent representation of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes.