Anatomy & Physiology: The Unity of Form and Function, 7th Edition

Published by McGraw-Hill Education
ISBN 10: 0073403717
ISBN 13: 978-0-07340-371-7

Chapter 12 - Section 12.4 - Electrophysiology of Neurons - Before You Go On - Page 455: 15

Answer

An action potential is a rapid, transient change in the membrane potential of a neuron, where the membrane potential briefly becomes more positive before returning to its resting state. The rise to +35 mV and the subsequent drop in membrane potential during an action potential are primarily driven by the opening and closing of voltage-gated ion channels. Here's a simplified explanation of how this process occurs: **1. Rising Phase of Action Potential (+35 mV):** - **Depolarization:** The action potential begins with a depolarization phase. When a neuron receives a strong enough excitatory signal (usually in the form of graded potentials or synaptic input), voltage-gated sodium (Na+) channels in the neuron's membrane open in response to the depolarization. These channels allow a rapid influx of sodium ions into the neuron, causing the membrane potential to become less negative (more positive). - **Threshold Reached:** As sodium ions flow into the neuron, the membrane potential becomes less negative and approaches a critical threshold level, typically around -55 to -50 mV. When this threshold is reached, it triggers a positive feedback loop that leads to the rapid opening of a large number of voltage-gated sodium channels. - **Sodium Influx:** The opening of these sodium channels results in a massive influx of sodium ions into the neuron. This influx of positive charge rapidly depolarizes the membrane, causing the membrane potential to rise sharply. It can reach values as high as +35 mV. **2. Falling Phase of Action Potential (After +35 mV):** - **Repolarization:** After reaching its peak at around +35 mV, the action potential enters its falling phase. This phase is driven by the opening of voltage-gated potassium (K+) channels and the inactivation of sodium channels. Potassium channels open more slowly than sodium channels. - **Potassium Efflux:** Voltage-gated potassium channels allow potassium ions to flow out of the neuron. As potassium ions leave the cell, the membrane potential starts to repolarize, moving back toward its resting potential, typically around -70 mV. - **Hyperpolarization:** In some cases, the membrane potential may briefly hyperpolarize, going below the resting potential. This is due to the slow closure of potassium channels, which briefly overshoot their equilibrium potential. - **Return to Resting Potential:** Eventually, potassium channels close completely, and the sodium channels return from their inactivated state to a closed state. This allows the neuron to return to its resting membrane potential, ready to transmit another action potential if the appropriate stimulus is received. In summary, the rise to +35 mV during an action potential is primarily due to the rapid influx of sodium ions, while the drop and repolarization phase are driven by the efflux of potassium ions and the inactivation of sodium channels. This sequence of events is highly regulated and essential for the propagation of electrical signals in neurons.

Work Step by Step

An action potential is a rapid, transient change in the membrane potential of a neuron, where the membrane potential briefly becomes more positive before returning to its resting state. The rise to +35 mV and the subsequent drop in membrane potential during an action potential are primarily driven by the opening and closing of voltage-gated ion channels. Here's a simplified explanation of how this process occurs: **1. Rising Phase of Action Potential (+35 mV):** - **Depolarization:** The action potential begins with a depolarization phase. When a neuron receives a strong enough excitatory signal (usually in the form of graded potentials or synaptic input), voltage-gated sodium (Na+) channels in the neuron's membrane open in response to the depolarization. These channels allow a rapid influx of sodium ions into the neuron, causing the membrane potential to become less negative (more positive). - **Threshold Reached:** As sodium ions flow into the neuron, the membrane potential becomes less negative and approaches a critical threshold level, typically around -55 to -50 mV. When this threshold is reached, it triggers a positive feedback loop that leads to the rapid opening of a large number of voltage-gated sodium channels. - **Sodium Influx:** The opening of these sodium channels results in a massive influx of sodium ions into the neuron. This influx of positive charge rapidly depolarizes the membrane, causing the membrane potential to rise sharply. It can reach values as high as +35 mV. **2. Falling Phase of Action Potential (After +35 mV):** - **Repolarization:** After reaching its peak at around +35 mV, the action potential enters its falling phase. This phase is driven by the opening of voltage-gated potassium (K+) channels and the inactivation of sodium channels. Potassium channels open more slowly than sodium channels. - **Potassium Efflux:** Voltage-gated potassium channels allow potassium ions to flow out of the neuron. As potassium ions leave the cell, the membrane potential starts to repolarize, moving back toward its resting potential, typically around -70 mV. - **Hyperpolarization:** In some cases, the membrane potential may briefly hyperpolarize, going below the resting potential. This is due to the slow closure of potassium channels, which briefly overshoot their equilibrium potential. - **Return to Resting Potential:** Eventually, potassium channels close completely, and the sodium channels return from their inactivated state to a closed state. This allows the neuron to return to its resting membrane potential, ready to transmit another action potential if the appropriate stimulus is received. In summary, the rise to +35 mV during an action potential is primarily due to the rapid influx of sodium ions, while the drop and repolarization phase are driven by the efflux of potassium ions and the inactivation of sodium channels. This sequence of events is highly regulated and essential for the propagation of electrical signals in neurons.
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