General Neuroscience

Basics of Neuroscience II: An Introduction to Internal Neural Communication

Alexander Skvortsov, William Ellsworth, Jacob Umans

    Hello, readers of YNCA Journal, and welcome back to the Basics of Neuroscience course, presented by the YNCA Executive Board. In last week’s lesson, we discussed the basic structure of neurons. We also touched upon basic neural communication, discussing synapses and neurotransmitters. In this edition, we will go further in depth discussing neural communication; specifically, we plan to emphasize electrical forces involved with these functions.

    As we discussed in the last edition, the brain is composed of 80 to 100 billion neurons, linked in a contiguous system. These neurons are cells just like any other. However, they also perform the function of transmitting messages throughout the nervous system. They are able to do this due to two branched structures called the dendrite and the axon, which function as input and output systems respectively.


Action Potentials

    A neuron firing is usually interpreted as the action potential. An action potential, or a neural output signal, is binary. A neuron either fires, or it doesn’t.  This concept is known as all-or-none firing, and it is an extremely important phenomenon in neural signaling.   

    Action potentials are electrical events.  Neurons, like all other cells, have different concentrations of ions (charged particles) inside the cell and outside the cell.  This charge difference creates a voltage (also known as electric potential) across the cell membrane (the thin layer separating the inside and outside of the cell).  

    In an action potential, certain transmembrane proteins, or proteins that have components both inside and outside of the cell membrane, are activated.  These proteins are called ion channels, and, when activated, they allow ions to diffuse down their concentration gradients.  This movement changes the voltage across the cell membrane. If the cell is depolarized enough, meaning that the charge of the cell relative to the extracellular medium rises to a value close enough to zero, an action potential will be initiated. The resting potential of a neuron -70 mV, and if the voltage reaches about -55mV (the threshold) an action potential is initiated. At the axon hillock, all inputs into the neurons (discussed later) are integrated; if the charge in this region of the neuron crosses the threshold, an action potential is generated.

    The first step in the creation of an action potential is the opening of voltage-gated sodium channels, or ion channels that allow sodium ions to enter the neuron, causing a massive increase in the voltage (which can reach up to 30mV).  Then, voltage-gated potassium channels, which are much slower to respond to changes in voltage, are activated. Potassium ions flow out of the cell, and eventually the voltage drops below -70mV in a process known as hyperpolarization.  Ultimately, the voltage returns to -70mV, and after a brief period or rest known as the refractory period, during which sodium channels are physically unable to reopen, the activated region of the neuron neuron is ready to produce another action potential. During this time, an ion pump known as Na+/K+-ATPase works to restore the concentration of Na+ as well as K+ to their base levels.

    Action Potentials travel through the axon using a process known as saltatory conduction. We already discussed that axons are coated with a lipid layer known as myelin in order to insulate the electrical signal, with gaps in between called Nodes of Ranvier. During saltatory conduction, ions entering sodium channels at one Node of Ranvier diffuse past the myelinated region to depolarize the next region to continue propagating the action potential. Overall, this allows the action potential to skip from one Node of Ranvier to the next, thus greatly increasing speed of conduction. One interesting feature  about saltatory conduction is that the signal can only move in one direction, unlike most other transmission processes when the signal spreads out wherever possible. This phenomenon is caused by the inability of sodium channels to propagate signals during its refractory period—once the refractory period is over, the charge in the cell is unable to cause another action potential.


Postsynaptic Potentials

    After the action potential fires, the signal is transferred to the dendrite of the receiving neuron through a process called synaptic transmission, but more on that in the next edition. Basically, chemicals called neurotransmitters are released upon firing which then react with the receiving neuron, triggering a signal called the Postsynaptic Potential. Unlike the action potential, the voltage of the Postsynaptic Potential can vary. This depends on the number of neurotransmitters released.

    Another major difference is the existence of both Excitatory Postsynaptic Potentials (EPSPs) alongside Inhibitory Postsynaptic Potentials (IPSPs). As discussed previously, whether or not an action potential is released is determined by changes in the voltage across the cell membrane. The membrane voltage change is primarily set by the sum of all incoming Postsynaptic Potentials. Charges from all EPSPs and IPSPs from different parts of the postsynaptic dendrite are added together to produce the total membrane voltage. This is known as spatial summation. Now, the purpose of IPSPs becomes clear. IPSPs allow for inhibition of an action potential. This can be crucial at the right time. For example, let’s consider a basic muscle movement. An alpha motor neuron fires, which triggers contraction of a muscle fiber. Now, without inhibition control, the antagonist muscles would remain in their relative states, whether that be contracted or relaxed. This would result in muscle tearing. However, the antagonist muscle receives an inhibitory charge, which allows muscle movement without damage.

    Similarly to spatial summation, there is a process called temporal summation. This is when a high occurrence of Postsynaptic Potentials build upon each other, allowing the charge to reach the threshold for activation more easily.

    One final basic principle to consider in terms of Postsynaptic Potentials is signal deterioration. When a PSP is released on the dendrites, the charge dissipates as it travels along the dendrite towards the soma. As a result, the signal that factors into spatial summation will be much weaker than they were upon first affecting the neuron. Because of this, inputs from several neurons are necessary to pass the threshold voltage and initiate an action potential. This allows for many thousands of neurons to contribute to calculations of a single neuron without completely frying it. Using this process, individual neurons act in a manner similar to microprocessors, working together to evaluate data and perform operations with it.


  1. Byrne, J. H. and Dafny, N. (eds.), Neuroscience Online: An Electronic Textbook for the Neurosciences Department of Neurobiology and Anatomy, The University of Texas Medical School at Houston (UTHealth) © 1997, all rights reserved.

Alexander Skvortsov

Alexander Skvortsov

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William Ellsworth

William Ellsworth

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Jacob Umans

Jacob Umans

Jacob Umans is an aspiring physician-scientist in the Stanford University Class of 2020. As a cofounder of the IYNA, he is passionate about science education and hopes to share his excitement about all subfields of neuroscience -- especially glial biology and neuroimmunity -- with students around the world. He hopes to go on to earn an MD/Ph.D. after graduating from Stanford and to use his clinical experience develop a research focused on developing a better understanding of and improved therapies for neurodegenerative diseases. Outside of neuroscience, Jacob is an avid fan of puns, table tennis, and reading.