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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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Muscarinic acetylcholine receptors The muscarinic acetylcholine receptor (MAR) is a G protein– coupled receptor whose activation leads to opening of K+channels and subsequent hyperpolarization of the plasma membrane2. The binding of acetylcholine leads to the activation of a G protein, which binds to and releases ion channels. These ion channels can allow a varity of ions to move in or out of the cell, including K+, Na+ and Ca2+.

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Thus the gradients push potassium ions out of the axon, helping the membrane potential go back to its value at rest. As the resting potential goes back to its original value, it is temporarily hyperpolarized due to the potassium ions just leaving and causing the charge between the inside and outside to differ more than resting potential (the inside is seemingly more negative in comparison to the outside).The resting potential is restored after the potassium ions diffuse away, even though the distributions of Na+ and K+ differ from what they were before the process. This is where the sodium-potassium pump comes back to reestablish the concentrations of the ions before the action

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Na+ and Cl- also contribute to reaching equilibrium. When the neuron is at equilibrium its charge is –70mV. If the cell gets a potassium leak it will use a sodium potassium pump in order to maintain the equilibrium. The way the pump works is buy using ATP to pump three sodium ions for every two potassium ions. Generation of action potential Action potential occurs when the neuron goes from equilibrium and depolarizes causing the neuron to become more positive. If the neuron depolarizes enough it will reach the threshold.

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These relax and tense in synchronization to contract and relax the entire muscle to which they belong. what is the stimulus for calcium to be released from the sarcoplamic reticulum? This stimulus is the from acetylcholine, a neurotransmitter, synthesized in in the cytoplasm of the motor neuron. Acetylcholine diffuses quickly across the synaptic cleft and binds to certain protein molecules. This increases membrane permeability to sodium ions.

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