How can threshold potential be reached

Neuroscientists use other words, such as a "spike" or an "impulse" for the action potential. The action potential is an explosion of electrical activity that is created by a depolarizing current.

This means that some event a stimulus causes the resting potential to move toward 0 mV. When the depolarization reaches about mV a neuron will fire an action potential. This is the threshold. If the neuron does not reach this critical threshold level, then no action potential will fire. Also, when the threshold level is reached, an action potential of a fixed sized will always fire There are no big or small action potentials in one nerve cell - all action potentials are the same size.

Action potentials are caused when different ions cross the neuron membrane. A stimulus first causes sodium channels to open. Because there are many more sodium ions on the outside, and the inside of the neuron is negative relative to the outside, sodium ions rush into the neuron.

Remember, sodium has a positive charge, so the neuron becomes more positive and becomes depolarized. It takes longer for potassium channels to open. When they do open, potassium rushes out of the cell, reversing the depolarization. Also at about this time, sodium channels start to close. This causes the action potential to go back toward mV a repolarization.

Graham, Editor. Author information Article notes Copyright and License information Disclaimer. Received Jan 26; Accepted Jun 3. Copyright Platkiewicz, Brette. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

This article has been cited by other articles in PMC. Abstract In central neurons, the threshold for spike initiation can depend on the stimulus and varies between cells and between recording sites in a given cell, but it is unclear what mechanisms underlie this variability.

Author Summary Neurons communicate primarily with stereotypical electrical impulses, action potentials, which are fired when a threshold level of excitation is reached.

Introduction Spike initiation in neurons follows the all-or-none principle: a stereotypical action potential is produced and propagated when the neuron is sufficiently excited, while no spike is initiated below that threshold. Results What is the spike threshold? Spike threshold in vitro In a typical in vitro experiment, one measures the response of the cell to a controlled stimulus, whose strength is defined by a parameter e.

Open in a separate window. Figure 1. Spike threshold definitions. Spike threshold in vivo Since the input to the neuron is not directly controlled in vivo, the concept of spike threshold does not have exactly the same meaning as in vitro. Figure 2. Relationships between spike threshold definitions. Spike threshold in models It might seem confusing that the definition of the voltage threshold is ambiguous and that most modulation effects that have been reported in the literature seem to apply to spike onset rather than spike threshold.

The threshold equation Sodium channel activation Cells excitability is generally due to the presence of voltage-gated sodium channels [49]. Figure 3. Influence of Na activation characteristics on spike threshold. Sodium channel inactivation and other conductances The threshold can also be modulated by sodium channel inactivation and by the many other ion channels that can be found in neurons [56] — [58].

Figure 4. Threshold dynamics To derive the threshold equation, we made a quasi-static approximation, assuming that all mechanisms that modulate the threshold are slow processes compared to the timescale of spike initiation. Sodium inactivation Several authors have hypothesized that Na inactivation is responsible for experimentally observed threshold variability in vivo [12] , [15] , [16] , [21].

Figure 5. Dynamical spike threshold. Voltage-dependent conductances In the same way, the dynamics of voltage-dependent conductances translates into threshold dynamics. Synaptic conductances Finally, synaptic conductances fluctuate in vivo , which also impacts the instantaneous value of the threshold, through the following equation:. Na channel density in the AIS Spikes could be initiated in the AIS rather than in the soma because of higher Na channel density [66] , [69] — [71] , or lower Na half-activation voltage V a [72] in the first segment.

Accuracy of the threshold equation Threshold dynamics in a single-compartment model To evaluate the quality of the threshold equation, we first simulated a biophysical single-compartment model with fluctuating synaptic conductances, mimicking the effect of synaptic activity in vivo.

Figure 6. Predicted versus measured dynamical threshold. Figure 7. Threshold variability and Na channel inactivation in a single-compartment model. Threshold prediction in a realistic multicompartmental model of spike initiation We then checked the accuracy of the threshold equation with a realistic multicompartmental model of spike initiation, where action potentials are initiated in the axon [54].

Figure 8. Accuracy of the threshold equation in a multicompartmental model of spike initiation [ 54 ]. Discussion The spike threshold differs between cells and for different types of stimulations [2] , [15] , [32] , [33] , [35]. Mechanisms for threshold modulation and variability Since Na channels are responsible for the generation of action potentials, the threshold is firstly determined by their activation characteristics. Approximations in the threshold equation To derive the threshold equation, we made several simplifying assumptions.

Figure 9. Fitting the Na activation curve to a Boltzmann function. Figure Experimental difficulties in the measurement of Na activation curves. Sharpness of spikes and threshold variability Spikes look sharper in the soma than in the AIS, presumably because they are initiated in the AIS and back-propagated to the soma [10] , [13] , [14].

Materials and Methods Membrane equation We consider a single-compartment neuron model with voltage-gated sodium channels and other ion channels voltage-gated or synaptic , driven by a current I. Exponential approximation With instantaneous activation, the sodium current is:. Dynamic threshold The effect of Na inactivation on the threshold can be seen in the exponential model above, neglecting other conductances thus. Numerical simulations We compared our theoretical predictions with numerical simulations of a previously published point-conductance model with fluctuating synaptic inputs [83].

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This makes the postsynaptic neuron less responsive to glutamate released from the presynaptic neuron. Short-term synaptic plasticity acts on a timescale of tens of milliseconds to a few minutes.

Short-term synaptic enhancement results from more synaptic terminals releasing transmitters in response to presynaptic action potentials.

Synapses will strengthen for a short time because of either an increase in size of the readily- releasable pool of packaged transmitter or an increase in the amount of packaged transmitter released in response to each action potential. Depletion of these readily-releasable vesicles causes synaptic fatigue. Short-term synaptic depression can also arise from post-synaptic processes and from feedback activation of presynaptic receptors. Long-term potentiation LTP is a persistent strengthening of a synaptic connection, which can last for minutes or hours.

These receptors are normally blocked by magnesium ions. Activated AMPA receptors allow positive ions to enter the cell. Therefore, the next time glutamate is released from the presynaptic membrane, it will have a larger excitatory effect EPSP on the postsynaptic cell because the binding of glutamate to these AMPA receptors will allow more positive ions into the cell. The insertion of additional AMPA receptors strengthens the synapse so that the postsynaptic neuron is more likely to fire in response to presynaptic neurotransmitter release.

Some drugs co-opt the LTP pathway; this synaptic strengthening can lead to addiction. In this situation, calcium that enters through NMDA receptors initiates a different signaling cascade, which results in the removal of AMPA receptors from the postsynaptic membrane. With the decrease in AMPA receptors in the membrane, the postsynaptic neuron is less responsive to the glutamate released from the presynaptic neuron.

The weakening and pruning of unused synapses trims unimportant connections, leaving only the salient connections strengthened by long-term potentiation. Privacy Policy. Skip to main content. The Nervous System.

Search for:. How Neurons Communicate. Nerve Impulse Transmission within a Neuron: Resting Potential The resting potential of a neuron is controlled by the difference in total charge between the inside and outside of the cell. Learning Objectives Explain the formation of the resting potential in neurons.

Key Takeaways Key Points When the neuronal membrane is at rest, the resting potential is negative due to the accumulation of more sodium ions outside the cell than potassium ions inside the cell.

Potassium ions diffuse out of the cell at a much faster rate than sodium ions diffuse into the cell because neurons have many more potassium leakage channels than sodium leakage channels. Sodium-potassium pumps move two potassium ions inside the cell as three sodium ions are pumped out to maintain the negatively-charged membrane inside the cell; this helps maintain the resting potential.

Key Terms ion channel : a protein complex or single protein that penetrates a cell membrane and catalyzes the passage of specific ions through that membrane membrane potential : the difference in electrical potential across the enclosing membrane of a cell resting potential : the nearly latent membrane potential of inactive cells.

Nerve Impulse Transmission within a Neuron: Action Potential Signals are transmitted from neuron to neuron via an action potential, when the axon membrane rapidly depolarizes and repolarizes. Learning Objectives Explain the formation of the action potential in neurons.

Key Takeaways Key Points Action potentials are formed when a stimulus causes the cell membrane to depolarize past the threshold of excitation, causing all sodium ion channels to open.

When the potassium ion channels are opened and sodium ion channels are closed, the cell membrane becomes hyperpolarized as potassium ions leave the cell; the cell cannot fire during this refractory period.

The action potential travels down the axon as the membrane of the axon depolarizes and repolarizes. Myelin insulates the axon to prevent leakage of the current as it travels down the axon. Nodes of Ranvier are gaps in the myelin along the axons; they contain sodium and potassium ion channels, allowing the action potential to travel quickly down the axon by jumping from one node to the next.

Key Terms action potential : a short term change in the electrical potential that travels along a cell depolarization : a decrease in the difference in voltage between the inside and outside of the neuron hyperpolarize : to increase the polarity of something, especially the polarity across a biological membrane node of Ranvier : a small constriction in the myelin sheath of axons saltatory conduction : the process of regenerating the action potential at each node of Ranvier.

Synaptic Transmission Synaptic transmission is a chemical event which is involved in the transmission of the impulse via release, diffusion, receptor binding of neurotransmitter molecules and unidirectional communication between neurons.

Learning Objectives Describe the process of synaptic transmission. Key Takeaways Key Points In a chemical synapse, the pre and post synaptic membranes are separated by a synaptic cleft, a fluid filled space.

The neurotransmitter termination can occur in three ways — reuptake, enzymatic degradation in the cleft and diffusion. Signal Summation Signal summation occurs when impulses add together to reach the threshold of excitation to fire a neuron. Learning Objectives Describe signal summation. Key Takeaways Key Points Simultaneous impulses may add together from different places on the neuron to reach the threshold of excitation during spatial summation. When individual impulses cannot reach the threshold of excitation on their own, they can can add up at the same location on the neuron over a short time; this is known as temporal summation.

The action potential of a neuron is fired only when the net change of excitatory and inhibitory impulses is non-zero. Key Terms temporal summation : the effect when impulses received at the same place on the neuron add up spatial summation : the effect when simultaneous impulses received at different places on the neuron add up to fire the neuron axon hillock : the specialized part of the soma of a neuron that is connected to the axon and where impulses are added together.

Synaptic Plasticity Synapses experience plasticity by strengthening or weakening over time. Learning Objectives Distinguish between long-term potentiation and long-term depression. Key Takeaways Key Points Short-term synaptic enhancement occurs when the amount of available neurotransmitter is increased, while short-term synaptic depression occurs when the amount of vesicles with neurotransmitters is decreased.

Synapses are strengthened in long-term potentiation LTP when AMPA receptors which bind to negatively-charged glutamate are increased, allowing more calcium ions to enter the cell, causing a higher excitatory response.