recap

44.2 recap

Neurons have membrane potentials due to ion concentration differences across their membranes and the different permeabilities of the membrane to those ions created by ion channels. Leak channels generate the resting potential, and opening and closing of gated channels can create graded changes in membrane potentials depending on how many of which channel types open or close. Voltage-gated channels have threshold potentials for opening. If some voltage-gated Na+ channels open, they create a local depolarization that brings other Na+ channels to threshold—a positive feedback mechanism that generates APs. Sudden closure of Na+ channels and the opening of K+ channels terminate the AP. APs are rapid, all-or-none changes in membrane potential that are conducted along axons from the cell body to the axon terminals. In myelinated axons, APs jump between nodes of Ranvier and conduction is more rapid than in nonmyelinated axons.

learning outcomes

You should be able to:

  • Demonstrate an understanding of how a membrane potential can be calculated based on intra- and extracellular ion concentration differences and relative permeabilities of the membrane to those ions.

  • Describe how graded membrane potentials enable a neuron to integrate various inputs.

  • Explain what changes in ion channels in the axonal membrane are responsible for different components of the action potential.

  • Explain how action potential conduction velocity is related to myelination and axon diameter, and why conduction of action potentials is unidirectional.

Question 1

Why does the Goldman equation produce a more accurate calculation of membrane resting potential than the Nernst equation?

The Nernst equation calculates the membrane potential that will exist across a membrane due to the movement of a specific ion across that membrane, given the concentration difference of that ion on the two sides of the membrane. The dominant ion responsible for the membrane resting potential is K+, but the potential calculated from the K+ concentrations by the Nernst equation does not equal the measured membrane potential. This is because the membrane is also slightly permeable to other ions, and they contribute to the measured membrane potential. The Goldman equation predicts membrane potential more accurately because it takes into account all ions that have concentration differences across the membrane as well as the relative permeability of the membrane to those ions.

Question 2

How do graded membrane potentials enable the activity in the axon of a neuron to integrate the various dendritic inputs to that neuron?

Inhibitory inputs to the dendrites of a neuron cause hyperpolarization of the dendrite membrane, and excitatory inputs cause depolarization. These changes in membrane potential spread to the neuron’s cell body. The resulting membrane potential of the cell body is a graded membrane potential because it is always reflecting the sum of the dendritic inputs. That graded membrane potential spreads to the base of the axon, which fires action potentials if its membrane potential reaches threshold for its electrically gated Na+ channels. Therefore the rate of action potential generation is a function of the graded membrane potential of the neuron’s cell body, hence an integration of all of the dendritic inputs.

Question 3

Why is an action potential self-regenerating?

When the voltage-gated Na+ channels open in a patch of membrane, that patch depolarizes. That local depolarization spreads by electrical conduction to neighboring regions of membrane, bringing them to threshold and thereby causing their electrically gated Na+ channels to open and regenerating that action potential. This process continues down the length of the axon.

Question 4

A clinical nerve conduction velocity test electrically stimulates a nerve at one location and records the muscle response at a more distal location. Why is this test used when a physician suspects a demyelinating disease?

If the axons of the motor neurons that stimulate the muscle are demyelinated, the conduction velocity will be decreased and reflected in a longer delay for the muscle to respond to the electrical stimulation.

Having described how APs are generated and transmitted along axons, we will next address the question of what happens when an AP reaches the axon terminal. How is its signal communicated to the next cell—which could be another neuron, a muscle cell, or a secretory cell?