Outside Electrode with Action Potential

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When an action potential occurs, the charge outside the neuron reverses in polarity to become negative. This reversal is due primarily to the rapid flow of positively-charged, sodium ions into the neuron.

Following an action potential, the membrane channels that opened to let positive sodium ions into the neuron close and remain closed for a brief time. During this absolute refractory period, another action potential cannot be triggered.

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The electrical potential change that results in the propagation of an action potential is called depolarization (reduction of polarization). This state of greater negativity inside the neuron is due to the outflow of positively-charged, potassium ions. This all-or-none response is characterized by the consistent size and timing of action potentials, regardless of the intensity of the initiating stimulus. As long as the neuron is moved to threshold, approximately 15 millivolts from resting potential, an action potential of brief duration will occur.

Hyperpolariztion (increased polarization) is the electrical condition associated with the absolute refractory period. Information in the nervous system is conveyed, therefore, based on the rate at which action potentials are initiated. Because the duration of the refractory period is approximately one millisecond, the fastest rate of impulse propagation along a neuron is about 1,000 per second.

Local anesthetics such as Novocain and Xylocaine function by attaching to the Na+ gates of the neuronal membrane, and thus prevent the flow of Na+ into the cell and the generation of an action potential upon stimulation. General anesthetics such as ether and chloroform function in a different fashion. These drugs decrease brain activity by opening K+ gates; thus allowing these ions out of the cell. The neuron becomes hyperpolarized as in the absolute refractory period, and is unable to discharge.