The Importance Of Resting Membrane Potential

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Resting Membrane Potential
When a neuron is not transmitting a signal, it is at rest. During resting potential, between the inside and outside of the neuron there is an ion displacement. The inside of the neuron is negative in comparison to the outside. The outside of the cell has a positive charged sodium and negatively charged chlorine, while potassium, positively charged, is more heavily charged inside the cell. This difference in the charge of sodium, chloride, and potassium maintains the dynamic equilibrium in the neuron. The ions attempt to keep equilibrium of the inside and outside of the membrane, but because the cell membrane allows only some ions to pass through the ion channels it cannot. These channels are based on ion selectivity,
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It is essential that they are not leaking potassium out. This is prevented by a pump that uses energy (ATP) to move three sodium ions out for every two potassium ions put into the neuron. You finally reach resting potential when the forces balance the electrical charge and the change of voltage of the neuron is measured. Resulting that the inside of the neuron is 70mV less than outside, meaning the resting membrane potential of a neuron is -70mV.
Generation of Action Potential
Neurons communicate through nerve impulses. The neural impulses generated from an action potential are “all or nothing,” meaning the signal reaches the threshold for communication or it doesn’t. There is no signal that is neither stronger nor weaker than the other. An action potential is a vast change in membrane potential, ultimately resulting in a +100mV swing in membrane potential. Neurons react to mechanical and chemical stimuli by generating small changes in the resting membrane potential called graded potentials.
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In fact, myofilaments slide past one another due to the increase of calcium ions and the cell shortens. The flow of calcium in the synaptic vesicles begins the excitation process when acetylcholine is released into the synaptic cleft by a motor neuron at the neuromuscular junction. The acetylcholine activated the flow of sodium ions and out flow of potassium ions, in result the end plate of the membrane potential is raised. This moves it close to threshold. Voltage gated calcium channels in the sarcolemma are opened by the end plate threshold and then rush into the axon terminal. The calcium released from the terminal cisternae of the sarcoplasm reacts on troponin, which exposes the myosin-binding site. The myosin heads latch on to the actin exposing active binding site, which form cross bridges. This is a series of events during which the myosin heads pull thin filaments toward the center of the sarcomere, resulting in the sliding of myofilaments (Marieb/Hoehn, 2014). This continues as long as ATP is available, as well as, sodium is bound to troponin, in result leaving the muscle cells un-relaxed. Each contraction becomes stronger until the nervous stimulation

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