Name: how ion channels shape neuron firing
Uploaded: 2023-04-30T10:12:08.000Z
Duration: 1 min 19 s
Channel: JoVE

A neuron&#39;s somatodendritic region can receive excitatory and inhibitory inputs from other neurons. All these EPSPs and IPSPs are summed at the axon hillock, and a decision is made whether to pass on the information to the next neuron.
This neuronal computation is aided by several voltage-gated channels present in the axon hillock and other neuron regions.
If the summation of postsynaptic signals fails to depolarize the membrane above the threshold, an action potential is not initiated. If the EPSP stimulation is above the threshold, voltage-gated sodium channels at the axon hillock depolarize the membrane to trigger the action potential.
For continued firing, delayed potassium channels repolarize the membrane, allowing another round of depolarization.
Additionally, rapidly inactivating potassium channels maintain the intensity and frequency of firing proportional to the strength of depolarization.
Through saltatory conduction, the signal moves along the axon and is finally transmitted&#160; to the next neuron.

the role of ion channels in neuronal computation

The Role of Ion Channels in Neuronal Computation

A postsynaptic neuron usually receives numerous impulses from several other presynaptic neurons. The axon hillock of the postsynaptic neuron integrates all these signals and determines the likelihood of firing an action potential.
Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron. However, multiple presynaptic inputs must often create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential. This process is called summation and occurs at the axon hillock. Whereas summation is temporal when the presynaptic neuron fires impulses in rapid succession. In a spatial summation, a postsynaptic neuron gets stimulated simultaneously by numerous presynaptic neurons.
Additionally, one neuron often has inputs from many presynaptic neurons, which can be excitatory or inhibitory&#8212;so IPSPs can cancel out EPSPs and vice versa. The net change in postsynaptic membrane voltage determines whether the postsynaptic cell has reached its threshold of excitation needed to fire an action potential. Together, synaptic summation and the threshold for excitation act as a filter so that random &#34;noise&#34; in the system is not transmitted as important information.
The movement of three ions: sodium, potassium, and calcium, across the ion channels is responsible for voltage sensing, ion permeability, and the overall neuronal integration for the action potential propagation.
Sodium (Na+) Channels
Voltage-gated Na+ channels concentrated in the axon&#39;s initial segment and the Nodes of Ranvier allow the action potential initiation and propagation. These channels have an open, closed, and inactive conformation. In the closed and inactive states, the channel is impermeable to ion. This ion-impermeable state is essential for opening other channels that help in action potential propagation.
Potassium (K+) Channels
Numerous types of potassium channels are seen distributed in the soma, dendrites, juxtaparanodes, and nodes of the neuron that work to ensure the propagation of the impulse.
Delayed K+channels open only when the voltage-gated Na+ channels are not activated. Hence they are &#39;delayed&#39; with respect to the Na+ current or Na+ ion flow, as these open slowly.
Rapid or fast inactivating K+-channels are inactive at resting membrane potential. When the membrane is sufficiently negative, these become available. In this way, they prolong the period between action potentials, thus maintaining the firing frequency.
A-type voltage-gated K+channels are rapidly inactivating channels that modulate the backpropagation of the action potential to the soma and dendrites. These channels help filter and shape electrical signals traveling between synapses and the soma and back from soma to synapses, preventing excessive firing.
Ca2+-activated K+channels are essentially potassium channels gated by voltage and raised calcium levels. The voltage-gated Ca2+ channels increase calcium levels and activate the K+ channels. The efflux of potassium ions makes membrane depolarization harder, allowing a delay between subsequent action potentials. Thus the neuron becomes less responsive to constant stimuli.
Calcium (Ca2+) Channels
Calcium channels are present on the axon terminals, soma, and dendrites. Voltage-gated Ca2+channels help release neurotransmitters from the presynaptic axon terminal. These also help in membrane depolarization by allowing calcium ion influx in the soma and dendrites.

A postsynaptic neuron usually receives numerous impulses from several other presynaptic neurons. The axon hillock of the postsynaptic neuron integrates ...

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Channels and the Electrical Properties of Membranes

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how ion channels shape neuron firing

Ion channels help neurons decide when to fire an action potential. A postsynaptic neuron often receives signals from many presynaptic neurons, and the axon hillock adds those inputs together to judge whether firing is likely. In some cases, one strong EPSP, or excitatory postsynaptic potential, is enough to trigger a spike. In many cases, several EPSPs must arrive close together for the cell to reach threshold.

This signal adding process is called summation. It can be temporal when one presynaptic neuron fires many impulses in quick succession. It can also be spatial when several presynaptic neurons stimulate the same postsynaptic neuron at the same time. Excitatory and inhibitory inputs both matter, because IPSPs, or inhibitory postsynaptic potentials, can cancel EPSPs and vice versa.

The net change in membrane voltage tells the postsynaptic cell whether it has reached the threshold for excitation. This threshold acts like a filter, so random noise is less likely to pass as important information. The movement of sodium, potassium, and calcium through ion channels supports this electrical integration and action potential propagation.

Voltage-gated sodium channels are concentrated in the axon initial segment and the Nodes of Ranvier. They allow action potentials to start and spread. These channels can be open, closed, or inactive. In the closed and inactive states, they do not let ions pass, and that impermeable state is important for opening other channels that support impulse propagation.

Potassium channels are found in the soma, dendrites, juxtaparanodes, and nodes of the neuron. Delayed potassium channels open only after voltage-gated sodium channels are not activated, so they open slowly and later than the Na+ current. Fast inactivating potassium channels are inactive at resting membrane potential and become available when the membrane is sufficiently negative. They help keep a delay between action potentials and support firing frequency. A-type voltage-gated potassium channels are rapidly inactivating and help control backpropagation of the action potential to the soma and dendrites. They shape signals between synapses and the soma and help prevent excessive firing. Ca2+-activated potassium channels respond to voltage and higher calcium levels. Voltage-gated calcium channels raise calcium levels, which then activates these K+ channels. The potassium efflux makes depolarization harder and creates a delay before the next action potential, so the neuron becomes less responsive to constant stimuli.

Calcium channels are present on the axon terminals, soma, and dendrites. In axon terminals, voltage-gated calcium channels help release neurotransmitters from the presynaptic neuron. In the soma and dendrites, they also support membrane depolarization by allowing calcium ions to enter the cell.

How Ion Channels Shape Neuron Firing

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Learn how sodium, potassium, and calcium ion channels help neurons sum signals, reach threshold, and trigger action potentials in high school biology.

How Ion Channels Shape Neuron Firing | JoVE K12

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How Ion Channels Shape Neuron Firing

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