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5.3: Synaptic Transmission

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    Learning Objectives

    1. Describe ion channels, and what changes they undergo when neuron potentials are produced; what causes ion channels to change during synaptic transmission?
    2. Define ionotropic and metabotropic receptors and discuss in what ways they differ from one another in their effects during synaptic transmission
    3. Explain the steps in synaptic transmission from pre-synaptic neuron to post-synaptic neuron
    4. Describe how excitatory and inhibitory transmitters differ in their effects on post-synaptic neurons during synaptic transmission
    5. Discuss how layers of neurons, simulated by processing units in artificial neural networks, might produce psychological processes such as learning


    After an action potential is generated in the presynaptic neuron, this all or none impulse is conducted along the axon to the axon ending (the terminal button). In the presynaptic terminal button, the arrival of the action potential triggers the release of neurotransmitters (see Figure 5.3.2). Neurotransmitters cross the synaptic gap and open subtypes of receptors in a lock-and-key fashion (see Figure 5.3.2). Depending on the type of neurotransmitter, an EPSP or IPSP occurs in the dendrite of the post-synaptic cell. Neurotransmitters that open Na+ or calcium (Ca+) channels cause an EPSP; an example is the NMDA receptors, which are activated by glutamate (the main excitatory neurotransmitter in the brain). In contrast, neurotransmitters that open Cl- or K+ channels cause an IPSP; an example is gamma-aminobutryric acid (GABA) receptors, which are activated by GABA, the main inhibitory neurotransmitter in the brain. Once the EPSPs and IPSPs occur in the postsynaptic site, the process of communication within and between neurons cycles on (see Figure 5.3.3). A neurotransmitter that does not bind to receptors is broken down and inactivated by enzymes or glial cells, or it is taken back into the presynaptic terminal button in a process called reuptake (Figure 5.3.2, Step 6).


    The transmission of neural messages across the synaptic gap, via the release of transmitter from a pre-synaptic neuron onto post-synaptic receptor sites on a post-synaptic neuron, is called synaptic transmission or neurotransmission. Synaptic transmission is central to the brain's capacity to process information, to generate mental states, and to generate adaptive behavior. Some synapses are purely electrical and make direct electrical connections between neurons (for example, between basket cells in the cerebellum). However, most synapses are chemical synapses, involving neurotransmitters. The transmission of neural signals across chemical synapses is more complex than at electrical synapses and involves many steps.

    Electrical Synapses

    Electrical synapses are much less common than chemical synapses, but they are nevertheless distributed throughout the brain. In chemical synapses neurotransmitter is needed for communication between neurons, but for electrical synapses this is not the case. In electrical synapses current, ions, and molecules can flow between two neurons through direct physical connections that allow cytoplasm to flow between them. The physical connection between neurons with electrical synapses is in the form of large pore structures, called connexons, at gap junctions between such neurons. Communication between neurons with electrical synapses is faster than at chemical synapses which must go through more steps to transmit signals to another neuron. Therefore, electrical synapses are often found in neural systems that require rapid response such as defensive reflexes. Electrical synapses can communicate signals in both directions between neurons in contrast to chemical synapses which transmit messages in one direction, from pre-synaptic by transmitter release to post-synaptic neuron.

    File:Gap cell junction-en.svg

    Figure \(\PageIndex{1}\): Gap junction at an electrical synapse. Two adjacent neurons with electrical synapse between them can communicate through hydrophilic channels Note that the gap between cell membranes of pre and post-synaptic neurons at electrical synapses is much smaller than the synaptic gap at chemical synapses which is about 10 times larger. (Image from Wikimedia Commons; File:Gap cell junction-en.svg; by Mariana Ruiz LadyofHats.; by Mariana Ruiz LadyofHats; public domain by its author, LadyofHats).

    Chemical Synapses

    We discussed previously which ions are involved in maintaining the resting membrane potential. Not surprisingly, some of these same ions are involved in the action potential. When the cell becomes depolarized (more positively charged) and reaches the threshold of excitation, this causes a voltage-dependent Na+ channel to open. A voltage-dependent ion channel is a channel that opens, allowing some ions to enter or exit the cell, depending upon when the cell reaches a particular membrane potential (i.e. a particular voltage).

    When the cell is at resting membrane potential, these voltage-dependent Na+ channels are closed. As we learned earlier, both diffusion from concentration gradients and electrostatic pressure from charge gradients are pushing Na+ ions toward the inside of the cell. However, Na+ cannot permeate the membrane when the cell is at rest.

    Once these channels are opened when trigger threshold has been reached, Na+ rushes inside the cell, causing the cell to become very positively charged relative to the outside of the cell. This is responsible for the rising or depolarizing phase of the action potential (see Module 5.2). The inside of the cell becomes very positively charged, from about +30mV to about +60mv, depending upon the particular neuron. At this point, the Na+ channels close and become refractory. This means the Na+ channels cannot reopen again until after the cell returns to the resting membrane potential. Thus, a new action potential cannot occur during the refractory period. The refractory period also ensures the action potential can only move in one direction down the axon, away from the soma.

    As the cell becomes more depolarized, a second type of voltage-dependent channel opens; this channel is permeable to K+. With the inside of the cell very positive relative to the outside of the cell (depolarized) and the high concentration of K+ within the cell, both the force of diffusion, along concentration gradients, and the force of electrostatic pressure, along charge gradients, drive K+ outside of the cell. The movement of K+ out of the cell causes the cell potential to return back to the resting membrane potential; this is the falling or hyperpolarizing phase of the action potential (see Module 5.2).

    A short hyperpolarization occurs partially due to the gradual closing of the K+ channels. With the Na+ channels closed, electrostatic pressure from a K+ charge gradient continues to push K+ out of the cell. In addition, the sodium-potassium pump is pushing Na+ out of the cell. The cell returns to the resting membrane potential, and the excess extracellular K+ diffuses away. This exchange of Na+ and K+ ions happens very rapidly, in less than one millisecond. The action potential occurs in a wave-like motion down the axon until it reaches the terminal button. Only the ion channels in very close proximity to the action potential are affected, causing the action potential to be regenerated along the axon--this creates the movement of the action potential down the axon.

    The binding of a neurotransmitter to its receptor is reversible, and for good reason. As long as it is bound to a post synaptic receptor, a neurotransmitter continues to affect membrane potential, so must be removed from the synapse. The effects of the neurotransmitter generally lasts a few milliseconds before being terminated. If the used transmitter is not removed or inactivated it can cause over-activation of neurons, potentially leading to pathological mental states and behavior if enough synapses are affected. Neurotransmitter termination can occur in three ways: First, reuptake by astrocytes or by the presynaptic terminal where the used transmitter can be destroyed by enzymes (Figure 5.3.2, step 6). Second, degradation by enzymes in the synaptic cleft such as the enzyme, acetylcholinesterase, which destroys used acetylcholine transmitter. Third, diffusion of the neurotransmitter as it moves away from the synapse. Again, destruction or removal of used transmitter from the synapse after it has done its work is essential to normal functioning of the nervous system.

    Microscopic image of an axon ending cut away to show synaptic vesicles inside the axon ending ready to release transmitter
    Figure \(\PageIndex{2}\): Synaptic vesicles inside a neuron: This pseudocolored image taken with a scanning electron microscope shows an axon terminal that was broken open to reveal synaptic vesicles (blue and orange) inside the neuron. (Image and caption adapted from: General Biology (Boundless), Chapter 35, The Nervous System;; LibreTexts content is licensed by CC BY-NC-SA 3.0. Legal).

    Ionotropic and Metabotropic Synapses

    There are two major categories of post-synaptic receptors: ionotropic receptors and metabotropic receptors.

    Ionotropic receptors, when activated by transmitter from a pre-synaptic neuron, cause ion channels to open, allowing ions, with their electrical charges, to move across the cell membrane of the receiving (post-synaptic) neuron, causing an EPSP or an IPSP (see above). These are fast acting receptors and are involved in the kind of neural transmission we have been describing above. Ionotropic receptors are receptors on ion channels that open, allowing some ions to enter or exit the cell, depending upon the presence of a particular neurotransmitter. The type of neurotransmitter and the permeability of the ion channel it activates will determine if an EPSP or IPSP occurs in the dendrite of the post-synaptic cell. These EPSPs and IPSPs summate and determine whether an action potential will be generated. For a video summary, copy and paste this web address into your browser:

    By contrast, metabotropic receptors (usually coupled with G-proteins; i.e. guanine nucleotide-binding proteins), when activated by transmitter from a pre-synaptic neuron, act indirectly and more slowly, using second messengers to produce a variety of metabolic effects to modulate cell activity. These effects include changes in gene transcription, regulation of proteins in the cell, release of Ca+ (calcium ions) within the cell, and effects on ion channels on the neuron's cell membrane (Sterling & Laughlin, 2015). Such modulation of neurons and synapses can be more long-lasting than effects of the activation of ionotropic receptors and may play an important role in cellular level mechanisms of learning and memory (Nadim and Bucher, 2014).

    File:1226 Receptor Types.jpg

    Figure \(\PageIndex{3}\): Comparison of Ionotropic and Metabotropic Post-Synaptic Receptors. The image at the top (a) shows ionotropic receptors which when activated by transmitter open ion channels immediately resulting in ion movement and an immediate response, a post-synaptic potential. The image at the bottom (b) shows metabotropic receptors which when activated by transmitter initiate a second messenger system. Second messengers can have a variety of effects including indirectly opening ion channels (Image from Wikimedia Commons; File:1226 Receptor Types.jpg;; by OpenStax; licensed under the Creative Commons Attribution 4.0 International license).

    8-Step Summary of Synaptic Transmission

    Here's a somewhat simplified but useful 8-step summary of the steps in synaptic transmission at synapses with ionotropic receptors:

    2) increased intracellular Ca+2 at the axon ending binds synaptic vesicles to pre-synaptic membrane triggering release of transmitter from synaptic vesicles in the axon ending of this pre-synaptic neuron

    3) molecules of neurotransmitter cross the fluid-filled synaptic space between pre- and post-synaptic neurons

    4) molecules of transmitter attach to post-synaptic ionotropic receptor sites on the dendrite or soma of the post-synaptic neuron on the other side of the synaptic space

    File:Generic Neurotransmitter System.jpg

    Figure \(\PageIndex{4}\): Image on left shows two neurons communicating with one another (synaptic transmission). The neuron at the top is the sender or pre-synaptic neuron. The neuron on the bottom is the receiver or post-synaptic neuron. In the image on the left of the figure, notice the small box at the synapse. This box is enlarged in the image on the right side of the figure to reveal details of the synapse and events there during synaptic transmission. The axon ending or bouton/button of the pre-synaptic neuron is at the top. We see transmitter molecules (small red squares) transported down the axon (arrow) from the cell body to the axon ending where they are stored in synaptic vesicles (yellow circles containing small red squares, i.e. transmitter molecules). When a nerve impulse (action potential) reaches the axon ending, calcium ions enter the axon ending/bouton/button causing synaptic vesicles to move to the axon ending's cell membrane (steps 1 and 2 referred to above) causing release of transmitter molecules into and across the synaptic gap (steps 2 and 3). Transmitter molecules bind to post-synaptic receptors (green) causing specific ion channels ("doors") to open to specific ions (steps 4 and 5). Ions (not shown in this figure) move through the ion channels in the post-synaptic neuron's cell membrane (step 6) with their electrical charges changing the voltage inside the post-synaptic neuron (either an EPSP or an IPSP). If trigger threshold (about negative 55 millivolts) is reached, an action potential is generated in the receiver neuron, which now becomes a sender neuron for the next cell in line (not shown in this figure). Inactivation of the used transmitter is the final step, step 8, and is depicted in this figure by "enzyme degradation" (enzymatic destruction). (Image from Wikimedia Commons; File:Generic Neurotransmitter System.jpg;; by NIDA(NIH); this work is in the public domain in the United States. Caption by Kenneth A. Koenigshofer, Ph.D.).

    5) this "lock and key" interaction, between transmitter molecules and the receptor sites that they attach to, "opens doors," that is, causes holes or pores (ion channels) in the post-synaptic neuron's cell membrane to open to specific ions (electrically charged atoms; sodium, chloride, potassium)

    6) ions move (along charge and concentration gradients) through specific ion channels across the cell membrane into or out of the post-synaptic neuron, carrying with them their electrical charges, altering the electrical potential inside the post-synaptic neuron (as noted above, this voltage shift is called a post-synaptic potential or PSP). If the transmitter is excitatory, then sodium channels open and sodium ions (Na+) follow the electric and charge gradients into the post-synaptic neuron making the voltage inside the neuron more positive (an EPSP). If the transmitter is inhibitory, think of chloride ions (Cl -) moving in and potassium ions (K+) moving out, making the inside of the post-synaptic neuron more negatively charged, moving the neuron's voltage further away from trigger threshold, thus inhibiting the neuron from firing (this is an IPSP). EPSPs and IPSPs can summate.

    7) if the voltage shift in the post-synaptic neuron is positive (an EPSP) and if it is large enough, or if summated inputs (summation) are positive enough to reach "trigger threshold" of the post-synaptic neuron (-55 millivolts), then Na+ channels suddenly open (voltage gated channels), Na+ rushes inside the cell, and an action potential is generated in the post-synaptic (receiver) neuron, which now becomes a pre-synaptic (sender) neuron for the next cell in line. The action potential is generated at the axon hillock and then is conducted down the length of the axon, jumping from node to node if the axon is myelinated. As the Na+ rushes inside the cell, this is responsible for the rising or depolarizing phase of the action potential (see Figure 5.3.2).

    8) Inactivation of used transmitter (by its reuptake into the pre-synaptic neuron or by its enzymatic destruction by specific enzymes)

    Drawings of chemical synapse illustrating steps in synaptic transmission, shows axon ending releasing transmitter. See text.

    Figure \(\PageIndex{5}\): Communication at a chemical synapse: Communication at chemical synapses requires release of neurotransmitters (refer to 8-step summary above). When the pre-synaptic membrane is depolarized, voltage-gated Ca2+ channels open and allow Ca2+ to enter the cell. The calcium entry causes synaptic vesicles to fuse with the membrane and release neurotransmitter molecules into the synaptic cleft. The neurotransmitter diffuses across the synaptic cleft and binds to ligand-gated ion channels (channels opened by chemical transmitter) in the post-synaptic membrane, resulting in a localized depolarization (EPSP) or hyperpolarization (IPSP) of the post-synaptic neuron depending upon the type of transmitter, excitatory or inhibitory. (Image and caption adapted from: General Biology (Boundless), Chapter 35, The Nervous System;; LibreTexts content is licensed by CC BY-NC-SA 3.0. Legal).

    Types of Neurotransmitter

    There are at least 60-100 neurotransmitters and probably many others yet to be discovered. The best known can be grouped into types based on their chemical structure.

    Today, the majority of neuroscientists will tell you that most neurons release the same neurotransmitter from their axons—which is why you may see some neurons referred to as “dopaminergic” or “serotonergic,” releasing dopamine or serotonin, respectively. But new work in the field has uncovered that neurons are not fixed when it comes to the chemicals they release.

    Some cells change the type of neurotransmitters they release depending on the circumstances, sometimes releasing up to five different kinds. Scientists call this phenomenon “neurotransmitter switching.”

    Neurotransmitters, at the highest level, can be sorted into two types: small-molecule transmitters and neuropeptides. Small-molecule transmitters, like dopamine and glutamate, typically act directly on neighboring cells. The neuropeptides, small molecules like insulin and oxytocin, work more subtly, modulating, or adjusting, how cells communicate at the synapse. These powerful neurochemicals are at the center of neurotransmission, and, as such, are critical to human cognition and behavior.

    Often, neurotransmitters are talked about as if they have a single role or function. Dopamine is a “pleasure chemical” and GABA is a “learning” neurotransmitter. But neuroscientists are discovering they are multi-faceted and complex, working with and against each other to facilitate neural signaling across the cortex. Here is a list of some of the most common neurotransmitters discussed in neuroscience.

    Amino acids neurotransmitters

    • Glutamate (GLU). This is the most common and most abundant excitatory neurotransmitter. Glutamate has an important role in cognitive functions like thinking, learning and memory. Too much glutamate results in excitotoxicity, or the death of neurons due to stroke, traumatic brain injury, or amyotrophic lateral sclerosis (ALS), the debilitating neurodegenerative disorder better known Lou Gehrig’s disease. GLU is also important to learning and memory: long term potentiation (LTP), occurs in glutamatergic neurons in the hippocampus and cortex.
    • Gamma-aminobutryic acid (GABA). GABA works to inhibit neural signaling. GABA is the most common inhibitory neurotransmitter in the nervous system, particularly in the brain. New research suggests that GABA helps lay down important brain circuits in early development. GABA also has a nickname: the “learning chemical.” Studies have found a link between the levels of GABA in the brain and whether or not learning is successful.
    • Glycine. Glycine is the most common inhibitory neurotransmitter in the spinal cord and is involved in auditory processing, pain and metabolism.

    Monoamines neurotransmitters

    Monoamines neurotransmitters are involved in consciousness, cognition, attention and emotion.

    • Serotonin (5HT). Serotonin is an inhibitory neurotransmitter. Serotonin helps regulate mood, sleep patterns, sexuality, anxiety, appetite and pain. Diseases associated with serotonin imbalance include seasonal affective disorder, anxiety, depression, fibromyalgia and chronic pain. Medications that regulate serotonin and treat these disorders include selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs), which increase the levels of transmitter by inhibiting their reuptake after they have done their work at the postsynaptic receptor sites. Serotonin (5HT), sometimes called the “calming chemical,” is best known for its mood modulating effects. A lack of 5HT has been linked to depression and related neuropsychiatric disorders. 5HT has also been implicated in facilitating memory, and, most recently, in decision-making behavior
    • Histamine. Histamine regulates body functions including wakefulness, feeding behavior and motivation.
    • Dopamine (DA). Dopamine is involved in the brain's reward system, feelings of pleasure, cognitive arousal, learning, focus of attention, concentration, memory, sleep, mood and motivation. Dopamine is often referred to as the “pleasure chemical” because it is released when mammals receive a reward in response to their behavior; that reward could be food, drugs, or sex. Diseases associated with dysfunctions of the dopamine system include Parkinson’s disease, schizophrenia, bipolar disease, restless legs syndrome and attention deficit hyperactivity disorder (ADHD). Many highly addictive drugs (cocaine, methamphetamines, amphetamines) act directly on the brain's dopamine circuits.
    • Epinephrine. Epinephrine (also called adrenaline) and norepinephrine (see below) are responsible for the “fight-or-flight response” to fear and stress, activating the sympathetic nervous system (see Chapter 4).
    • Norepinephrine (NE). Norepinephrine is both a hormone and a neurotransmitter. Some refer to it as noradrenalin. It has been linked to mood, arousal, vigilance, memory, and stress. Newer research has focused on its role in both post-traumatic stress disorder (PTSD) and Parkinson’s disease. Norepinephrine (noradrenaline) increases blood pressure, heart rate, alertness, arousal, attention and focus. Many medications (stimulants and depression medications) increase norepinephrine to improve focus or concentration to treat ADHD or to reduce symptoms of depression.

    Peptide neurotransmitters

    Peptides are short chains of amino acids.

    • Endorphins. Endorphins are natural pain killers. They are natural opiate-like substances, similar in molecular properties to morphine. Release of endorphins reduces pain, and elevates mood. They are endogenous opiates released by the hypothalamus and pituitary gland during stress or pain.

    Acetylcholine (ACh)

    This excitatory neurotransmitter is found in both the central and peripheral nervous systems, specifically in the autonomic nervous system and in spinal motor neurons releasing acetylcholine onto skeletal muscles producing movements. It is also involved in memory, motivation, sexual desire, sleep and learning. Abnormalities in acetylcholine levels are associated with Alzheimer’s disease. But it also has other roles in the brain, including helping direct attention and playing a key role in facilitating neuroplasticity across the cortex.

    Other Neurotransmitters

    Neurochemicals like oxytocin and vasopressin are also classified as neurotransmitters. Made and released from the hypothalamus, they act directly on neurons and have been linked to pair-bond formation, monogamous behaviors, and drug addiction. Hormones like estrogen and testosterone can also work as neurotransmitters and influence synaptic activity.

    Other neurotransmitter types include corticotropin-releasing factor (CRF), galanin, enkephalin, dynorphin, and neuropeptide Y. CRH, dynorphin, and neuropeptide Y have been implicated in the brain’s response to stress. Galanin, encephalin, and neuropeptide Y are often referred to as “co-transmitters,” because they are released and then work in partnership with other neurotransmitters. Enkephalin, for example, is released with glutamate to signal the desire to eat and process rewards.

    As neuroscientists are learning more about the complexity of neurotransmission, it’s clear that the brain needs these different molecules so it can have a greater range of flexibility and function.

    Glia Release Neurotransmitters, Too

    It was once believed that only neurons released neurotransmitters. New research, however, has demonstrated glia, the cells that make up the “glue” that fills the space between neurons to help support and maintain those cells, also have the power to release neurotransmitters into synapses. In 2004, researchers found that glial cells release glutamate into synapses in the hippocampus, helping synchronize signaling activity.

    Astrocytes, a star-shaped glial cell, are known to release a variety of different neurotransmitters into the synapse to help foster synaptic plasticity, when required. Researchers are working diligently to understand the contributions of these different cell types–and the neurotransmitter molecules they release—on how humans think, feel, and behave.

    Different Types of Receptors Activated by the Same Transmitter

    There are different types of receptor for transmitters of a specific type. For example, for dopamine there are at least 5 types, D1 through D5 receptors, all for dopamine transmitter. Different receptor types for a specific transmitter may be localized in different parts of the brain and therefore may produce different effects and have different functions.

    The function of each dopamine receptor type (Mishra, et al., 2018):

    • D1: memory, attention, impulse control, regulation of renal (kidney) function, locomotion (movement)
    • D2: locomotion, attention, sleep, memory, learning
    • D3: cognition, impulse control, attention, sleep
    • D4: cognition, impulse control, attention, sleep
    • D5: decision making, cognition, attention, renin secretion (by the kidney)

    Of particular interest, the mental disorder schizophrenia, characterized by disordered thought, hallucinations, and delusions, is associated with excess dopamine neuron activity in the brain. Some drug treatments for schizophrenia decrease activity primarily at D2 receptors.

    Another example is acetylcholine transmitter. There are two distinct types of acetylcholine receptors affected by two different substances, either muscarine or nicotine. Those postsynaptic acetylcholine receptors that respond to muscarine are called muscarinic receptors. Those that respond to nicotine (in tobacco products, for example) are called nicotinic. Nicotinic receptors cause sympathetic postganglionic neurons and parasympathetic postganglionic neurons to fire and release their chemicals and cause skeletal muscle to contract. Muscarinic receptors are associated mainly with parasympathetic functions and stimulate receptors located in peripheral tissues (e.g., glands, smooth muscle). Acetylcholine transmitter activates all of these sites.

    Synaptic Transmission in Review

    Let's summarize the sequence of events in synaptic transmission in synapses with ionotropic receptors:

    Action potential in pre-synaptic neuron --- transmitter release --- transmitter crosses synaptic gap --- transmitter attaches to post-synaptic receptor sites --- ion channels open --- ions move --- PSP results --- if the PSP is an EPSP and if the EPSP is big enough (or if summation results in voltage change big enough), then trigger threshold of -55mv is reached in post-synaptic neuron ---post-synaptic neuron produces its own action potential. These same steps are summarized in the first 7 of the 8 steps in synaptic transmission listed above. The last step is transmitter inactivation.

    Action potential causes transmitter release producing EPSPs or IPSPs; if trigger threshold is reached new action potential occurs.

    Figure \(\PageIndex{6}\): Summary of the electrochemical communication within and between neurons. (Image from Furtak, S. (2021). Neurons. In R. Biswas-Diener & E. Diener (Eds), Noba textbook series: Psychology. Champaign, IL: DEF publishers. Retrieved from

    Step 8 in the list of 8 steps above simply refers to the fact that after the released transmitter molecules have done their job, the used transmitter molecules must be cleaned out of the synapse. If not, the receiving neuron will be affected for too long and this may result in dysfunction at the synapse, resulting in pathological effects, and if occurring at a large number of synapses can lead to abnormalities such as seizures or hallucinations or other maladaptive effects.

    As noted above, removal of used transmitter is accomplished by two mechanisms, reuptake and enzymatic destruction. Reuptake means that the used transmitter is reabsorbed back into the pre-synaptic ending from which it was released. Enzymatic destruction means that the used transmitter is chemically destroyed by an enzyme, and thereby inactivated.

    If step 8, transmitter inactivation, didn't occur, in the case of excitatory transmitters, then the post-synaptic neuron would be over activated. If this occurs on a large scale, at many synapses, as noted above, behavioral and mental abnormalities will result. For example, there are some drugs (Soman, Sarin, Malathion) that block enzymatic destruction of the neurotransmitter Acetylcholine, ACh. As noted above, ACh is a transmitter involved in various functions in the brain and peripheral nervous system, including stimulation of skeletal muscles, which are responsible for movement. Soman and Sarin are nerve agents. They block the enzyme acetylcholinesterase, AChE, and thereby prevent the enzymatic destruction of ACh at motor synapses which stimulate the muscles. As a result, the excess ACh at the muscles causes their over activation. The result? Epileptic seizures so intense that death may occur. The treatment for poisoning by these agents is a drug that blocks acetylcholine neurotransmitter at the acetylcholine receptor sites, counteracting effects of the excess acetylcholine neurotransmitter, thereby preventing or reversing the seizures otherwise caused by these nerve agents.

    Neurons, The Mind, and Artifical Neural Networks

    How do these neural processes relate to the real world of our everyday conscious experience and behavior? As mentioned in module 5.2, in complex vertebrate species, single nerve cells and their activity do not control a behavior or create a thought or a feeling. Instead, information is processed, mental states are created, and behaviors are organized by neural events in complex circuits involving very large numbers of neurons. It is the interaction among huge numbers of neurons, interconnected by enormous numbers of synapses, that create our perceptions, thoughts, emotions, or a complex behavior such as human speech or the creation of a work of art.

    How groups of neurons in complex circuits might produce complex things like a perception or a memory has been studied using computer modeling (see Module 10.9). Artificial neural networks are computer-based models of neural circuits and their functioning. In a computer program, artificial information processing units, sometimes called "neurodes", are programmed to code and process information similar to how neurons process information. These neuron-like processing units are interconnected with one another and organized into layers, and then these layers of processing units are connected.

    A three-layered artificial neural network (see Module 10.9) is capable of performing some very complex information processing tasks, producing responses similar to those that a real brain might produce. Furthermore, because the artificial neurodes or processing units are given (by programmers) the capability of altering the strengths or "weights" of their "synaptic connections", artificial neural networks are capable of learning when given feedback about their performance. Given these properties, it has been shown by researchers (many of whom are at UC San Diego) that artificial neural networks can learn patterns and regularities in inputs to make generalizations, to form categories, and to solve complex problems (Churchland, 2013).

    For example, one neural network, trained (electronically) in the mathematical principles used to find mathematical proofs, discovered a proof that had eluded human mathematicians for many decades. Another, known as NETtalk, equipped with a voice synthesizer and photocell "eyes" learned from scratch to read and correctly pronounce written English text. It accomplished this astounding feat after only 10 hours of trial and error learning, during which it was given feedback about its attempts at pronunciation. It went through a babbling stage initially, like a child would, but soon was articulating comprehensible speech. When tested on new material, it generalized what it had learned to the new text including many new words that it had not "seen" before. An analysis by researchers of how it did this showed that it had formed categories of letters, learning to divide them into vowels and consonants, with rules of pronunciation for each category. It accomplished this without direct programming by humans. It extracted regularities from the words presented to it, and made generalizations, rules which it applied to new cases (Churchland, 2013).

    Artificial neural networks use a form of information processing called parallel distributed processing (PDP). Though these networks are not brains, they have come closer than any other computer models to simulating brain function and psychological capabilities of real brains. This suggests that biological brains may use PDP, carried out by PDP networks made of real neurons, to produce the kinds of psychological and behavioral capacities which real brains like ours demonstrate. This is a very promising area of research being carried out in the psychology, computer science, and neuroscience departments at many universities worldwide.

    Keep in mind that the circuitry in biological brains, such as the human brain, though modifiable by experience, is also hard-wired to a significant extent by natural selection and other forces of evolution (see Chapter 3). This accounts for the fact that human beings have an innate or inborn human nature just like other animals have their own innate natures. Humans relate to the world in a distinctively human way whereas wolves, tigers, birds, wildebeests, and other animal species understand and relate to the world in their own particular species-typical ways. Each species' distinctive psychological nature is a result of the brain circuitry inherited from its predecessors--circuitry molded by eons of evolution (Koenigshofer, 2011).


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    Chapter 5 Review

    1. Define nerve impulse.
    2. What is the resting potential of a neuron, and how is it maintained?
    3. Explain how and why an action potential occurs.
    4. Outline how a signal is transmitted from a presynaptic cell to a postsynaptic cell at a chemical synapse.
    5. What generally determines the effects of a neurotransmitter on a postsynaptic cell?
    6. Identify three general types of effects neurotransmitters may have on postsynaptic cells.
    7. Explain how an electrical signal in a presynaptic neuron causes the transmission of a chemical signal at the synapse.
    8. The flow of which type of ion into the neuron results in an action potential?
      1. How do these ions get into the cell?
      2. What does this flow of ions do to the relative charge inside the neuron compared to the outside?
    9. The sodium-potassium pump:
      1. is activated by an action potential
      2. requires energy
      3. does not require energy
      4. pumps potassium ions out of cells
    10. True or False. Some action potentials are larger than others, depending on the amount of stimulation.
    11. True or False. Synaptic vesicles from the presynaptic cell enter the postsynaptic cell.
    12. True or False. An action potential in a presynaptic cell can ultimately cause the postsynaptic cell to become inhibited.
    13. Name three neurotransmitters.

    Chapter 5 Discussion Questions

    1. What structures of a neuron are the main input and output channels of that neuron?
    2. What does the statement mean that communication within and between cells is an electrochemical process?
    3. How does myelin increase speed and efficiency of the action potential?
    4. How does diffusion (concentration gradients) and electrostatic pressure (electrical gradients) contribute to the resting membrane potential and the action potential?
    5. Describe the cycle of communication within and between neurons.

    Chapter 5 Vocabulary

    Action potential (nerve impulse)

    A transient all-or-nothing positive electrical current (depolarization) that is conducted down the axon when the membrane potential reaches the threshold of excitation (trigger threshold equal to about negative 55 millivolts).


    Part of the neuron that extends off the soma, splitting several times to connect with other neurons; main output of the neuron.

    Cell membrane

    A bi-lipid layer of molecules that separates the cell from the surrounding extracellular fluid.


    Part of a neuron that extends away from the cell body and is the main input to the neuron.

    Diffusion (along a concentration gradient or inequality)

    The force on molecules to move from areas of high concentration to areas of low concentration.

    Electrostatic pressure (charge gradient)

    The force on two ions with similar charge to repel each other; the force of two ions with opposite charge to attract to one another.

    Excitatory postsynaptic potentials (EPSPs)

    A graded depolarizing postsynaptic current that causes the membrane potential to become more positive and move towards the threshold of excitation (trigger threshold). EPSPs and IPSPs can summate with one another.

    Inhibitory postsynaptic potentials (IPSPs)

    A graded hyperpolarizing postsynaptic current that causes the membrane potential to become more negative and move away from the threshold of excitation (trigger threshold). EPSPs and IPSPs can summate with one another.

    Ion channels

    Proteins that span the cell membrane, forming channels that specific ions can flow through between the intracellular and extracellular space (the "doors" in step 5 in the list of 8 steps of synaptic transmission above; see Figure 5.3.2).

    Ionotropic receptor

    Receptor (receives transmitter molecules and binds to them) and its associated ion channel that opens to allow ions to permeate the cell membrane under specific conditions, such as the presence of a neurotransmitter (chemically-gated channel) or a specific membrane potential (voltage-gated channel).

    Myelin sheath

    Substance around the axon of a neuron that serves as insulation to allow the action potential to conduct rapidly toward the terminal buttons.

    Neurotransmitters or transmitters

    Chemical substance released by the presynaptic terminal button that acts on the postsynaptic cell.


    Collection of nerve cells found in the brain which typically serve a specific function.

    Resting membrane potential

    The voltage inside the cell relative to the voltage outside the cell while the cell is a rest (approximately -70 mV).

    Sodium-potassium pump

    An ion channel that uses the neuron’s energy (adenosine triphosphate, ATP) to pump three Na+ ions outside the cell in exchange for bringing two K+ ions inside the cell.


    Cell body of a neuron that contains the nucleus and genetic information, and directs protein synthesis.


    Protrusions on the dendrite of a neuron that form synapses with terminal buttons of the presynaptic axon.


    Junction between the presynaptic terminal button of one neuron and the dendrite, axon, or soma of another postsynaptic neuron.

    Synaptic gap or synaptic space

    Also known as the synaptic cleft; the small space between the presynaptic terminal button (axon ending) and the postsynaptic dendritic spine, axon, or soma.

    Synaptic vesicles

    Groups of neurotransmitters packaged together and located within the terminal button.

    Terminal button or axon ending

    The part of the end of the axon that form synapses with postsynaptic dendrite, axon, or soma.

    Trigger threshold (Threshold of excitation)

    Specific membrane potential that the neuron must reach to initiate an action potential.


    1. Chapter 5, Communication within the Nervous System, Module 5.3. Neurons and Synaptic Transmission by Kenneth A. Koenigshofer, PhD, Chaffey College, is licensed under CC BY 4.0

    2. "Types of Neurotransmitters" and "Glia Release Transmitters Too" adapted by Kenneth A. Koenigshofer from Sukel, K (2019) Neurotransmitters from

    2. Figure 5.3.3, Vocabulary, Discussion Questions, Outside Resources, and some text adapted by Kenneth A. Koenigshofer from Furtak, S. (2021). Neurons. In R. Biswas-Diener & E. Diener (Eds), Noba textbook series: Psychology. Champaign, IL: DEF publishers. Retrieved from

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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.

    3. Figures 5.3.1, 5.3.2 and some text adapted by Kenneth A. Koenigshofer from: General Biology (Boundless), Chapter 35.2C, The Nervous System; Synaptic Transmission,; LibreTexts content is licensed by CC BY-NC-SA 3.0. Legal.

    4. Figures 5.2.2 and "Chapter 5 Review" adapted by Kenneth A. Koenigshofer 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


    Outside Resources for Chapter 5

    Video Series: Neurobiology/Biopsychology - Tutorial animations of action potentials, resting membrane potentials, and synaptic transmission.
    Video: An animation and an explanation of an action potential

    Video: An animation of neurotransmitter actions at the synapse

    Video: An interactive animation that allows students to observe the results of manipulations to excitatory and inhibitory post-synaptic potentials. Also includes animations and explanations of transmission and neural circuits.
    Video: Another animation of an action potential

    Video: Another animation of neurotransmitter actions at the synapse

    Video: Domino Action Potential: This hands-on activity helps students grasp the complex process of the action potential, as well as become familiar with the characteristics of transmission (e.g., all-or-none response, refractory period).

    Video: For perspective on techniques in neuroscience to look inside the brain

    Video: The Behaving Brain is the third program in the DISCOVERING PSYCHOLOGY series. This program looks at the structure and composition of the human brain: how neurons function, how information is collected and transmitted, and how chemical reactions relate to thought and behavior.
    Video: You can grow new brain cells. Here\\\'s how. -Can we, as adults, grow new neurons? Neuroscientist Sandrine Thuret says that we can, and she offers research and practical advice on how we can help our brains better perform neurogenesis—improving mood, increasing memory formation and preventing the decline associated with aging along the way.

    Web: For more information on the Nobel Prize shared by Ramón y Cajal and Golgi

    This page titled 5.3: Synaptic Transmission is shared under a mixed license and was authored, remixed, and/or curated by Kenenth A. Koenigshofer (ASCCC Open Educational Resources Initiative (OERI)) .