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5.2: Neurons Generate Voltage Changes to Code Information

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    According to materialists (those who believe that everything in the universe is physical), all of the mental activities of our minds and all of our behaviors are products of the physical activities of the brain and nervous system. These information processing operations that create our minds and control our behavior depend upon neurons and their electrical and chemical interactions. Neurons produce electrical potentials (voltages) that act as signals in the information processing activities of the brain. As previously mentioned, neurons communicate with one another across synaptic spaces using chemicals known as neurotransmitters. In this module, we examine how neurons create electrical potentials including the graded potentials (post-synaptic potentials) and the nerve impulse (the action potential), and the processes of synaptic transmission. The graded potentials can vary in voltage, while the action potential is fixed in voltage for any particular neuron and is said to be all or none--if it occurs, it occurs at its full strength or not at all. This is analagous to the firing of a gun. It has a trigger threshold equal to a particular amount of pressure applied to its trigger and then that threshold pressure is reached, the gun fires, and it fires at its full "strength." In a like manner, the action potential will only be generated if its trigger threshold, a particular voltage within the neuron, is reached. When this happens, the action potential is generated in the neuron at its full "strength," measured in voltage, and this nerve impulse is conducted along the axon to the axon endings which then release neurotransmitter onto receptor sites located on the receiving neuron. We now examine these processes in greater detail in this module and the next.

    How Do Neurons Produce Electrical Potentials?

    As described in Module 5.1, neurons, regardless of type, use voltage changes, known as electrical potentials, to code and process information. But how do they do it? How do neurons make voltage which they then use as electrical signals in the brain's electrochemical code? More specifically, the question is, how do neurons produce electrical potentials such as the resting potential, the action potential, and the post-synaptic potentials?

    Neurons produce electrical potentials or voltages by the unequal distribution and the movement of electrically charged atoms called ions across the neuron's cell membrane. These ions come mainly from dissolved salts in the body fluids inside and outside neurons. The main ions used by neurons to produce their voltages are sodium (Na+), potassium (K+), and chloride (Cl-). Notice that the first two are positive ions and the last, chloride ions, are negatively charged. A fourth ion, organic anions (A-), which are large (on the molecular scale) negatively charged proteins, are manufactured inside the neuron. They are too large to cross the cell membrane, and therefore give the neuron's resting voltage a negative bias. The distribution or concentrations of these ions inside and outside a neuron determine its voltage (voltage is just the physical separation of charged particles, like in a car battery with its positive and negative poles around which are concentrated positively and negatively charged particles floating in battery acid).

    By these means, four main types of neuron voltages or neuron potentials are produced by neurons: 1) the resting potential (often equal to about negative 70 thousandths of a volt, -70 millivolts) 2) two types of post-synaptic potentials (PSPs)--excitatory post-synaptic potentials (EPSPs) and inhibitory post-synaptic potentials (IPSPs) and 3) the action potential (AP, the nerve impulse). Let's examine these potentials in more detail and see how they are generated inside neurons. These electrical potentials in large populations of interacting neurons encode the information that guides our behavior and produces our psychological experience of the world.

    The Neuron Cell Membrane

    The cell membrane, which is composed of a lipid bilayer of fat molecules, separates the fluid inside of the cell from the surrounding extracellular fluid. There are proteins that span the membrane, forming ion channels that allow, when open, particular ions to pass between the intracellular and extracellular fluid (see Figure 8). These ions are in different concentrations inside the cell relative to outside the cell, and the ions have different electrical charges. Due to this difference in ion concentration and charge, in part enforced by the physical barrier of the cell membrane when ion channels to specific ions are closed, a voltage is produced, the resting potential.

    The Resting Membrane Potential

    The resting potential can be thought of as a baseline voltage from which the other neuron potentials are generated. It is the voltage inside a nerve cell when it is at rest, that is, it is neither receiving inputs (PSPs) at the moment nor generating any outputs (action potentials) at the moment. In this state of "rest", the voltage inside the nerve cell is approximately -70 mv. It is negative inside the neuron at "rest" because there are more negative ions inside the neuron (the intracellular fluid) and more positive ions on the outside (the extracellular fluid).

    Specifically, there are large numbers of Na+ ions (sodium ions) outside the neuron and very few of these on the inside, when the neuron is "at rest" (when it is at resting potential). And there are more negatively charged ions inside the cell than on the outside during resting potential. This unequal distribution of ions across the cell membrane sets up the electrical "resting potential," making it equal to approximately -70 mv in the typical neuron. During resting potential (resting membrane potential) ion channels to Na+ are closed.

    Representation of ion concentrations inside (intracellular) and outside (extracellular) an axon at a node of Ranvier.  See text.

    Figure \(\PageIndex{1}\): Representation of ion concentrations inside (intracellular) and outside (extracellular) a neuron in the unmyelinated segment of the axon. Size of the circles represents relative concentrations of each ion inside and outside the neuron; note that when the neuron is "at rest" it has a net negative charge inside, the resting potential, equal to about -70 millivolts in most neurons. Also note the higher concentrations of sodium (Na+) and chloride (Cl-) ions outside the cell. Sodium on the outside of the neuron "would like" to move into the cell along its charge and concentration gradients, but it can't when the cell is at rest, because the ion channels for sodium ions are closed, creating a physical barrier keeping most of the extracellular sodium ions from crossing through the cell membrane. But what happens when the sodium channels open? And, test yourself, what opens the ion channels?

    The Sodium-Potassium Pump

    During the resting potential, the sodium-potassium pump maintains a difference in charge across the cell membrane of the neuron. The sodium-potassium pump is a mechanism of active transport that moves sodium ions out of cells and potassium ions into cells. The sodium-potassium pump moves both ions from areas of lower to higher concentration, using energy in ATP and carrier proteins in the cell membrane (see Figure 5.2.2).

    Scheme of sodium potassium pump

    Figure \(\PageIndex{2}\): The sodium-potassium pump helps maintain the resting potential of a neuron. During resting potential, there is more negative charge inside than outside the cell creating a resting potential of -70mv. During resting potential, some Na+ leaks into the neuron and some K+ leaks out. ATP (Adenosine triphosphate) provides energy to pump sodium out and potassium into the cell. There is more concentration of sodium outside the membrane and more concentration of potassium inside the cell due in part to the unequal movement of these ions by the pump. The presence of negatively charged organic anions (A-) contributes to the net negative charge (-70mv) inside the neuron at rest. (Image from Wikimedia Commons; File:Scheme sodium-potassium pump-en.svg;; by LadyofHats Mariana Ruiz Villarreal; released into the public domain by its author, LadyofHats. This applies worldwide).

    Producing Other Membrane Potentials: Post-synaptic potentials and the Action potential

    How are the other neuron potentials produced? To generate the other neuron potentials, which are just voltage shifts away from resting potential, there must occur a redistribution of ions (and their electrical charges) across the cell membrane. In short, ions must move.

    There are two main forces (called gradients) that can cause these ions to move.

    First, opposite charges attract one another ("opposites attract"), and like charges repel one another. When ions of opposite charge are unequally distributed across the cell membrane (as is the case during the resting potential), this sets up what is called a charge gradient (an unequal distribution of charged particles) that creates an electrostatic force. If these ions are allowed to move freely, they will move along the charge gradient. Positive charges will move toward negative ones and vice versa.

    Secondly, when ions of any particular type (for example, sodium ions) are unequally distributed across the cell membrane (like more Na+ outside the neuron than inside during resting potential), this sets up what is called a concentration gradient which can cause diffusion, the net movement of ions from a region of higher concentration to a region of lower concentration. Diffusion is driven by a gradient in concentration. Such concentration gradients for several ions (sodium, potassium, and chloride ions) exist when the neuron is at resting potential (see Figure 10). Ions, if allowed to move freely, will move along their concentration gradients, such that ions of a particular type (like Na+ ions) will move from a region of high concentration (of Na+) to a region of lower concentration (of Na+).

    In short, ions, if allowed to move freely, will move along the charge gradient and along their concentration gradients. Ions "want" to move to equalize their concentrations across the cell membrane and also "want" to move to equalize the charges across the cell membrane (by moving toward opposite charges and away from like charges).

    However, it is important to note that these two forces created by the charge gradient and concentration gradient for each ion can oppose one another in the case of some ions, or can act in concert (as is the case with Na+ ions during the resting potential).

    Let us see how these two forces, diffusion (due to concentration gradients) and electrostatic pressure (due to a charge gradient), act on the four groups of ions mentioned above.

    1. Anions (A-): Anions are highly concentrated inside the cell and contribute to the negative charge of the resting membrane potential. Diffusion and electrostatic pressure are not forces that determine A- concentration because A- is impermeable to the cell membrane. There are no ion channels that allow for A- to move between the intracellular and extracellular fluid.
    2. Potassium (K+): The cell membrane is very permeable to potassium at rest, but potassium remains in high concentrations inside the cell. Diffusion created by the concentration gradient pushes K+ to the outside of the cell because it is in high concentration inside the cell. However, electrostatic pressure created by the charge gradient pushes K+ into the cell because the positive charge of K+ is attracted to the negative charge inside the cell. In combination, these forces oppose one another with respect to K+ with the charge gradient (opposite charges attract) overpowering the concentration gradient so that the net effect is to push and keep K+ inside the neuron in higher concentrations.
    3. Chloride (Cl-): The cell membrane is also very permeable to chloride at rest, but chloride remains in high concentration outside the cell. Diffusion created by a concentration gradient for Cl- pushes Cl- toward the inside of the cell because it is in high concentration outside the cell. However, electrostatic pressure created by the charge gradient for Cl- pushes Cl- toward the outside of the cell because the negative charge of Cl- is attracted to the positive charge outside the cell created primarily by the high concentration of Na+ there. Similar to K+, these forces oppose one another with respect to Cl- and again, in this case, like Na+, the more powerful charge gradient (like charges repel) overcomes the weaker concentration gradient for Cl-.
    4. Sodium (Na+): The cell membrane is not very permeable to sodium when the neuron is at rest. Diffusion created by a concentration gradient pushes Na+ toward the inside of the cell because it is in high concentration outside the cell. Electrostatic pressure created by the charge gradient for Na+ also pushes Na+ toward the inside of the cell because the positive charge of Na+ is attracted to the negative charge inside the cell. Both of these forces push Na+ inside the cell; however, as discussed above, Na+ cannot permeate the cell membrane because the channels for Na+ are closed and so Na+ remains in high concentration outside the cell. The small amounts of Na+ inside the cell are removed by the sodium-potassium pump (Figure 5.2.2), which uses the neuron’s energy (adenosine triphosphate, ATP) to pump three Na+ ions out of the cell in exchange for bringing two K+ ions inside the cell.

    Though ions "want" to move in these ways dictated by their charge gradients and concentration gradients, Na+ can't move freely when the neuron is at resting membrane potential because Na+ ion channels are closed and the cell membrane acts as a physical barrier to Na+ ions, preserving the unequal distributions of Na+ ions inside and outside the neuron. To get ion movement, pores or ion channels in the cell membrane of the neuron "at rest" must be opened, overcoming the physical barrier created by the cell membrane when the neuron is "at rest" (not receiving any inputs via its dendrites and not generating any outputs, action potentials, via its axon) and its sodium channels are closed.

    What is it that causes the ion channels to open, allowing the ions to move along their gradients? You can test yourself here to see how much you have retained from your reading thus far. What is it that opens the ion channels?

    The arrival of transmitter molecules from the axon ending of a pre-synaptic neuron, and their attachment to post-synaptic receptor sites, is the key event. This "lock and key" interaction between molecules of transmitter and the post-synaptic receptor sites causes "doors", specific ion channels, to open.

    When specific ion channels get opened in this way (Na+ channels, for example), those specific ions (Na+, in this case) move through the cell membrane along their specific concentration and charge gradients. This will cause a voltage shift away from resting potential. This voltage shift is the post-synaptic potential (PSP), in this case it is an excitatory post-synaptic potential (EPSP), a positive shift in voltage away from resting potential because when Na+ channels in the cell membrane are opened by neurotransmitter, then Na+ ions will move along their charge gradient and concentration gradient into the cell, making the inside of the neuron more positively charged.

    Excitatory and Inhibitory Post-Synaptic Potentials
    1. Excitatory postsynaptic potentials (EPSPs): a depolarizing current that causes the membrane potential to become more positive and closer to the threshold of excitation (the "trigger threshold" of minus 55 millivolts) which lead to generation of an action potential (see Figure 5.2.4); caused by excitatory transmitter.
    2. Inhibitory postsynaptic potentials (IPSPs): a hyperpolarizing current that causes the membrane potential to become more negative (see Figure 5.2.4) and further away from the threshold of excitation (the "trigger threshold" of minus 55 millivolts), caused by inhibitory transmitter.

    The post-synaptic potentials occur in a post-synaptic neuron (thus the name), a receiver neuron. When such a neuron receives an input from a pre-synaptic neuron, in the form of transmitter molecules which attach to the post-synaptic receptor sites (which are proteins that are embedded in the membrane of the post-synaptic cell), ion channels then open, ions move across the cell membrane, carrying with them their electrical charges. These events change the voltage inside the post-synaptic neuron. It is this voltage shift away from resting potential that constitutes the post-synaptic potential (PSP).

    An EPSP (Excitatory Post-synaptic Potential) is a positive shift in voltage (depolarization) from the resting potential, say from -70 mv to -60 mv; as described above, an EPSP occurs when Na+ channels open and Na+ ions flow into the neuron along their concentration and charge gradients, carrying with them their positive charges, making the interior of the post-synaptic neuron more positively charged. This positive shift in voltage is also known as depolarization of the neuron and is caused by excitatory transmitter molecules binding to post-synaptic receptor sites of the receiving neuron.

    An IPSP (Inhibitory Post-synaptic Potential) is a negative shift in voltage (hyperpolarization) from the resting potential, say from -70 mv to -80 mv; an IPSP occurs when Cl- and K+ channels open. These ions then flow along charge and concentration gradients, which cause negatively charged Cl- ions to move in and positively charged K+ ions to move out of the post-synaptic neuron, making it more negatively charged. This increase in net negative charge inside the cell is the IPSP (inhibitory post-synaptic potential). Cl- ions move in against their charge gradient (the negative voltage of the resting potential repels Cl- ions) because the concentration gradient pushing them inward into the neuron is stronger than the opposing charge gradient that tries to push them out of the neuron (like charges repel). Similarly, K+ ions move out in opposition to the charge gradient pulling them in, again, because the concentration gradient pulling them outward is stronger than the charge gradient which tries to pull them inward. These movements are prevented during the resting potential by the added physical barrier, the cell membrane, but when these ion channels are opened more than they are during the resting potential, the gradients move the ions causing the IPSP. As noted above, in the case of Na+ both charge and concentration gradients pull Na+ inward when Na+ ion channels in the neuron's cell membrane open.

    Note, again, that in both the EPSP and the IPSP, it is the attachment of molecules of transmitter to post-synaptic receptor sites (like keys going into locks of a specific shape) that opens the "doors", the ion channels, allowing ions to move through the cell membrane.

    But there is one more key issue here. What is it that determines which ion channels open, and therefore, whether an EPSP or an IPSP occurs? The answer was implied above. The answer is: it is the type of neurotransmitter and type of receptor site receiving the transmitter molecules. There are two basic types of neurotransmitter, excitatory and inhibitory.

    Excitatory transmitters (such as glutamate, acetylcholine--ACh, norepinephrine--NE, dopamine--DA) are those which open sodium (Na+) channels in the post-synaptic membrane, allowing sodium ions, carrying their positive charge, into the cell, making an EPSP.

    Inhibitory transmitters (such as gamma-amino-butyric acid--GABA, serotonin--5-HT, or dopamine--DA) are those which affect chloride and potassium channels in the post-synaptic membrane, allowing chloride to follow its concentration gradient (overcoming the opposing charge gradient) into the post-synaptic neuron and allowing potassium to follow its concentration gradient (overcoming its opposing charge gradient) and moving out. These ion movements make the inside of the neuron more negative, making an IPSP.

    Notice that DA is listed as both excitatory and inhibitory. That's because some post-synaptic DA receptors are inhibitory, leading to IPSPs when activated by DA, and other DA receptors are excitatory, producing EPSPs when they bind with DA.

    Spatial and Temporal Summation

    There is one additional factor in this process. Each neuron connects with numerous other neurons, often receiving multiple impulses from them. Sometimes, a single excitatory postsynaptic potential (EPSP) is strong enough to induce an action potential in the postsynaptic neuron, but often multiple presynaptic inputs must create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential. Summation, either spatial or temporal, is the addition of these impulses at the axon hillock. Together, synaptic summation and the threshold for excitation act as a filter so that random “noise” in the system is not transmitted as important information.

    At any moment in time, each neuron can be receiving mixed messages, both EPSPs and IPSPs. Thus, receiver neurons (post-synaptic neurons) can receive multiple inputs--simultaneously or over time or space. The multiple inputs can add up--this is called summation and there are two types. Spatial summation refers to two or more PSPs arriving at different locations (i.e. different spaces on the receiving neuron, thus spatial summation) on the post-synaptic (receiver) neuron simultaneously or close enough in time so that their voltages add together. For example, an IPSP of negative 25 millivolts (thousandths of a volt) might add to an EPSP of 50 millivolts occurring at the same time = 50 millivolts positive - 25 millivolts = net positive 25 millivolts. That would be spatial summation. The other kind of summation is temporal summation when the PSPs from a single pre-synaptic source, arriving to the post-synaptic neuron in "rapid fire," add together. For example, three EPSPs of 10 millivolts each occurring in rapid sequence would add together. Spatial and temporal summation are important in determining whether "trigger threshold" will be reached in the receiving neuron, triggering an action potential in that neuron. Summation permits activity from many input neurons to be integrated in the neuron receiving the inputs. If membrane depolarization does not reach the threshold level, an action potential will not happen.

    Graph of voltage changes inside a postsynaptic neuron as EPSPs and IPSPs summate to reach trigger threshold. See text.
    Figure \(\PageIndex{3}\): Signal summation at the axon hillock: A single neuron can receive both excitatory and inhibitory inputs from multiple neurons. All these inputs are added together at the axon hillock. If the EPSPs are strong enough to overcome the IPSPs and reach the threshold of excitation, the neuron will fire an action potential. (Image from Biology, Signal Summation; Libretexts; Unless otherwise noted, LibreTexts content is licensed by CC BY-NC-SA 3.0).

    One neuron often has input from many presynaptic neurons, whether excitatory or inhibitory; therefore, inhibitory postsynaptic potentials (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 ("trigger threshold") needed to fire an action potential. If the neuron only receives excitatory impulses, it will also generate an action potential. However, if the neuron receives both inhibitory and excitatory inputs, the inhibition may cancel out the excitation and the nerve impulse will stop there. To review, spatial summation means that the effects of impulses received at different places on the neuron add up so that the neuron may fire when such impulses are received simultaneously, even if each input on its own would not be sufficient to cause firing. Temporal summation means that the effects of impulses received at the same place can add up if the impulses are received in close temporal succession. Thus, the neuron may fire when multiple inputs are received, even if each input on its own would not be sufficient to cause firing.

    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 additive effect when successive impulses (and the resulting PSPs) received at the same place on the neuron add up
    • spatial summation: the additive effect when simultaneous impulses (and the resulting PSPs) received at different places on the neuron add up
    • axon hillock: the specialized part of the soma of a neuron at the root of the axon where impulses are added together
    The Action Potential (the "nerve impulse")

    The nerve impulse, or action potential, is generated in the post-synaptic neuron only if a "trigger threshold" ("threshold of excitation") of -55 millivolts (minus 55 mv) is reached (the trigger threshold varies from neuron to neuron and may be anywhere from minus 65 to minus 55, but will always be the same for any particular neuron. For purposes of our discussion, we will continue to refer to the trigger threshold of neurons as minus 55 millivolts, not minus 65 as is sometimes indicated in some textbooks). When that trigger voltage is attained (for example, as a result of an EPSP of at least 15 millivolts), then all the voltage-gated sodium ion channels suddenly open, allowing a massive inflow of sodium ions, Na+, into the cell along both concentration and electrical gradients for sodium. This produces a rapid, large positive shift or "spike" in the voltage of the post-synaptic neuron. This is the nerve impulse or action potential. In most neurons, it is a positive shift of about 100 to 130 millivolts, if we measure from the -70 millivolts of the resting potential, up to about a positive 30 to 60 millivolts, depending on the neuron. This value for any particular neuron is always the same for that neuron. Typically neurons with larger diameters (such as A fibers which are typically myelinated as well as large diameter) produce the largest action potentials (up to about positive 60mv, i.e. 130 mv above resting potential), while the neurons with smaller diameter axons (classified as C fibers, typically unmyelinated) produce action potentials in the lower range.

    As fast as the voltage of the action potential rises, it starts to fall after reaching its peak (corresponding to peak Na+ concentration inside the neuron). It quickly falls back to the resting potential and even a bit below resting potential (the so-called refractory period), as Na+ and K+ ions move out, before the return of the neuron's potential back to -70 mv, the resting potential. This rapid rise to the action potential's peak and then its rapid fall gives the action potential, when graphed, a spike appearance. For this reason, action potentials are often called "spikes" by neuroscientists. See the diagram of the action potential (Figures 11, 12) to get a clearer picture of these events. Note that an EPSP, an excitatory post-synaptic potential, moves the neuron's voltage closer to "trigger threshold", increasing the chances that the neuron will be sufficiently "excited" to generate an action potential. By contrast, the IPSP, the inhibitory post-synaptic potential, moves the neuron's voltage further away from "trigger threshold" inhibiting the neuron from firing an action potential.

    Once trigger threshold ("threshold of excitation") is reached (dotted line in Figure 9) and an action potential is generated, it is then conducted down the length of this neuron's axon (saltatory conduction in a myelinated axon; see above). Once the AP reaches this neuron's axon ending or terminal button, its arrival causes the release of neurotransmitter molecules from the synaptic vesicles located there. Now this neuron is no longer called a post-synaptic neuron, but becomes a pre-synaptic neuron (a sender neuron) with respect to the next cell in line. It's the release of transmitter (step 3 in the list of 8 steps in synaptic transmission shown in Synaptic Transmission below) leads to steps (4 and 5 in the list of 8 steps) and an EPSP or IPSP is generated in the next cell in line. Remember that whether an EPSP or an IPSP is caused in the next cell in line is determined by whether an excitatory or an inhibitory transmitter has been released from the pre-synaptic neuron (see the 8 steps below).

    Resting potential is -70 mV; IPSP is a shift more negative; EPSP is a positive shift; at -55, action potential to +40 is triggered.

    Figure \(\PageIndex{4}\): Changes in membrane potentials of neurons. (left) Dotted line represents trigger threshold ("threshold of excitation"), about -55 millivolts, an action potential is generated once trigger threshold voltage is reached.

    Note that an EPSP (depolarization) moves the neuron's voltage more positive and thus closer to trigger threshold, making it more likely that the voltage reaches trigger threshold, "firing" an action potential down the axon of the neuron; thus it is excitatory. An IPSP does the opposite. It moves the voltage in the negative direction, further from trigger threshold, and thus inhibiting the neuron from producing an output (an action potential) in its axon. Also note that the peak of the action potential (top of the black line shaped like a spike) is the peak of its positive voltage and corresponds to the maximum concentration of Na+ ions inside the cell as a result of Na+ ion channels opening after trigger threshold has been reached. After this peak concentration of Na+ making the peak of the voltage of the action potential, positively charged ions (including K+ ions) begin to leave the interior of the cell and as they do so, the positive voltage inside the neuron progressively drops, corresponding to the downward slope of the spike. Note in addition that the spike goes further negative than the resting potential. In this state the neuron is inhibited by this refractory period and cannot fire another action potential for a brief time. This keeps the action potential as a discrete digital event. This is important for source coding, an important feature of neural coding, discussed in the chapter on learning and memory in this text. The entire process from the triggering of the action potential (which starts in the root of the axon, called the axon hillock, nearest the cell body) to the end of the refractory period takes about 1 millisecond, making the maximum rate at which a neuron can generate and "fire" action potentials (nerve "impulses") about 1,000 per second, although most neurons when active fire at a much lower frequency. Frequency of action potentials is one code that the nervous system uses to represent information. For example, the brighter a light source is, the higher the frequency of action potentials in the optic nerve in response to it.

    At left, graph of action potential with steps numbered; at right, graph of action potential shows ion movements. See text.File:مراحل ارسال سیگنال عصبی.jpg

    Figure \(\PageIndex{5}\): Formation of an action potential. (left) The formation of an action potential can be divided into five steps. (1) A stimulus from a sensory cell or another neuron causes the target cell to depolarize toward the threshold potential. (2) If the threshold of excitation is reached, all Na+ channels open and the membrane depolarizes. (3) At the peak action potential, K+ channels open and K+ begins to leave the cell. At the same time, Na+ channels close. (4) The membrane becomes hyperpolarized as K+ ions continue to leave the cell. The hyperpolarized membrane is in a refractory period and cannot fire. (5) The K+ channels close and the Na+/K+ transporter (requiring energy expenditure) restores the resting potential. (right) Sequence of opening and closing of Sodium (Na+) and Potassium (K+) ion channels producing the rising and falling phases of the action potential. (Image on left and caption from Lumen Boundless Biology; How Neurons Communicate; Unless otherwise noted, content is licensed under the Creative Commons Attribution 4.0 License. Image on right from Wikimedia Commons; File.مراحل ارسال سیگنال عصبی.jpg;; by Vidakarimnia; licensed under the Creative Commons Attribution-Share Alike 3.0 Unported license).

    A single neuron by itself can't generate psychological states like feelings, perceptions, or thoughts. Neurons must interact with other neurons. The generation of a thought, or other complex psychological/mental experience, requires that enormous numbers of neurons interact with one another. To interact, they must communicate with other neurons.

    As described in module 5.1, neurons communicate with one another, across spaces between them known as "synaptic gaps" by the release of chemicals (called neurotransmitters or simply transmitters) from one neuron's axon ending onto receptor sites on the dendrites or soma of the target neuron (a post-synaptic neuron). The neurotransmitters involved in this communication between neurons are manufactured in the soma of the neuron and are then transported down a long axon where they are stored in the synaptic vesicles until released from the axon ending into the synaptic space; the release is triggered by the arrival of an action potential (the nerve impulse) at the axon ending.

    As discussed in module 5.1, the synapse includes the pre-synaptic neuron (the sender cell) and its axon ending with its synaptic vesicles, along with the synaptic gap, and the post-synaptic neuron (the receiving cell) with its receptor sites. There are an enormous number of neurons in the human brain, but the number of possible different combinations of synaptic connections among those 80-100 billion neurons is unimaginable--one neuroscientist estimated that the number of possible patterns of interconnect between neurons in a human brain exceeds the number of atoms in the entire universe! This neural complexity appears to be sufficient to code all the information contained in a human brain including all the thoughts, feelings, perceptions and memories of a human lifetime.

    Key Points

    • The resting potential, typically equal to -70 millivolts, is the voltage inside a neuron when it is receiving no inputs from other neurons and producing no outputs (no action potentials)
    • Post-synaptic potentials (PSPs), EPSPs (excitatory; depolarizations) and IPSPs (inhibitory; hyperpolarizations) are positive and negative voltage shifts, respectively, away from the neuron's resting potential. These voltage shifts, PSPs, in the post-synaptic neuron result from release of transmitter from one or more pre-synaptic neurons.
    • Action potentials are formed when inputs (summed EPSPs and IPSPs) cause the cell membrane to depolarize past the threshold of excitation ("trigger threshold"), causing all sodium ion channels to open, leading to a large positive shift in the neuron's voltage (Figures 5.2.4 and 5.2.5).
    • 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 (Figures 5.2.4 and 5.2.5).
    • The action potential travels down the axon as the membrane of the axon depolarizes and repolarizes (see 5.1, Figures 5.1.4 and 5.1.5) .
    • Myelin insulates many axons to prevent leakage of the current as it "leaps" from node to node 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 (saltatory conduction; see module 5.1).

    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


    1. Chapter 5, Communication within the Nervous System, 5.2. "Neurons Generate Voltage Changes to Code Information" by Kenneth A. Koenigshofer, PhD, Chaffey College, is licensed under CC BY 4.0

    2. Figures 5.2.1, 5.2.4, Vocabulary, Discussion Questions, Outside Resources, and some text adapted from: Furtak, S. (2021). Neurons. In R. Biswas-Diener & E. Diener (Eds), Noba textbook series: Psychology. Champaign, IL: DEF publishers. Retrieved from; Neurons by Sharon Furtak at NOBA is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Figure 5.2.4 caption by Kenneth A. Koenigshofer, PhD, Chaffey College.

    3. "Key Points" and "Key Terms" adapted from: General Biology (Boundless), Chapter 35, The Nervous System;; LibreTexts content is licensed by CC BY-NC-SA 3.0. Legal.

    4. Figures 5.2.3, 5.2.5, and some text adapted from: General Biology (Boundless), Chapter 35, The Nervous System;; LibreTexts content is licensed by CC BY-NC-SA 3.0. Legal.

    5. Figures 5.2.2 adapted from Chapter 11.3 (Neurons and Glia Cells), 11.4 (Nerve Impulses) in Book: Human Biology (Wakim & Grewal) - Biology LibreTexts by Suzanne Wakim & Mandeep Grewal, under license CC BY-NC

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    Creative CommonsAttributionNon-CommericalShare-Alike Neurons by Sharon Furtak is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Permissions beyond the scope of this license may be available in our Licensing Agreement.

    This page titled 5.2: Neurons Generate Voltage Changes to Code Information is shared under a mixed license and was authored, remixed, and/or curated by Kenenth A. Koenigshofer (ASCCC Open Educational Resources Initiative (OERI)) .