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Acetylcholine Lab Report

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Glucose enters the nerve terminal by passive transport. Glycolysis occurs in the neuronal cytoplasm and pyruvate molecule are generated. Pyruvate is transported into the mitochondria and an acetyl group derived from pyruvic acid combines with coenzyme-A present in the mitochondria to form acetyl coenzyme-A, which is transported back into the cytoplasm. Choline is actively transported into the neuronal terminal from the synaptic cleft via sodium and choline transporters. An enzyme choline acetyltransferase (ChAT) in the nerve terminals synthesizes acetylcholine from choline and acetyl coenzyme A. After its synthesis, acetylcholine is packaged into vesicles and transported from the cytoplasm into synaptic vesicles by the vesicular acetylcholine …show more content…

The hypothesis of the experiment is that the injection of toxins and drugs that inhibit the release acetylcholine will cause paralysis and relaxation of the muscles and vice- versa. Five rats will be used for the experiment. Botulinum toxin, black widow spider venom, snake venom, curare and pilocarpine drug will be injected into the fore limb of the five rats. Electromyography will be used to monitor the contraction of the muscles. A needle electrode will be inserted directly into the muscle close to the injected area and the electrical activity of the muscle will be recorded with the electromyogram. The rats 1,3, 4 that were each injected with the botulinum toxin, snake venom and the curare respectively will experience less contraction and more relaxation of the muscles eventually leading to paralysis. In the rat ‘2’ injected with the black widow spider venom, the release of acetylcholine will not be suppressed but the rat will experience the wastage of the acetylcholine supplies and the muscles will begin to contract. When the acetylcholine supply is depleted, paralysis occurs. The injection of the pilocarpine drug on the rat 5, will lead to the contraction of the muscle, because the drug does not suppress the release of

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