17.2: Chemical and Electrical Synapses - Biology

17.2: Chemical and Electrical Synapses - Biology

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The synapse or “gap” is the place where information is transmitted from one neuron to another. There are two types of synapses: chemical and electrical.

Chemical Synapse

When an action potential reaches the axon terminal it depolarizes the membrane and opens voltage-gated Na+ channels. Na+ ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated Ca2+ channels to open. Calcium ions entering the cell initiate a signaling cascade that causes small membrane-bound vesicles, called synaptic vesicles, containing neurotransmitter molecules to fuse with the presynaptic membrane. Synaptic vesicles are shown in Figure 1, which is an image from a scanning electron microscope.

Fusion of a vesicle with the presynaptic membrane causes neurotransmitter to be released into the synaptic cleft, the extracellular space between the presynaptic and postsynaptic membranes, as illustrated in Figure 2. The neurotransmitter diffuses across the synaptic cleft and binds to receptor proteins on the postsynaptic membrane.

The binding of a specific neurotransmitter causes particular ion channels, in this case ligand-gated channels, on the postsynaptic membrane to open. Neurotransmitters can either have excitatory or inhibitory effects on the postsynaptic membrane. There are several examples of well known neurotransmitters detailed in Table 1. For example, when acetylcholine is released at the synapse between a nerve and muscle (called the neuromuscular junction) by a presynaptic neuron, it causes postsynaptic Na+ channels to open. Na+ enters the postsynaptic cell and causes the postsynaptic membrane to depolarize. This depolarization is called an excitatory postsynaptic potential (EPSP) and makes the postsynaptic neuron more likely to fire an action potential. Release of neurotransmitter at inhibitory synapses causes inhibitory postsynaptic potentials (IPSPs), a hyperpolarization of the presynaptic membrane. For example, when the neurotransmitter GABA (gamma-aminobutyric acid) is released from a presynaptic neuron, it binds to and opens Cl channels. Cl ions enter the cell and hyperpolarizes the membrane, making the neuron less likely to fire an action potential.

Once neurotransmission has occurred, the neurotransmitter must be removed from the synaptic cleft so the postsynaptic membrane can “reset” and be ready to receive another signal. This can be accomplished in three ways: the neurotransmitter can diffuse away from the synaptic cleft, it can be degraded by enzymes in the synaptic cleft, or it can be recycled (sometimes called reuptake) by the presynaptic neuron. Several drugs act at this step of neurotransmission. For example, some drugs that are given to Alzheimer’s patients work by inhibiting acetylcholinesterase, the enzyme that degrades acetylcholine. This inhibition of the enzyme essentially increases neurotransmission at synapses that release acetylcholine. Once released, the acetylcholine stays in the cleft and can continually bind and unbind to postsynaptic receptors.

Table 1. Neurotransmitters
Acetylcholinemuscle control, memoryCNS and/or PNS
Serotoninintestinal movement, mood regulation, sleepgut, CNS
Dopaminevoluntary muscle movements, cognition, reward pathwayshypothalamus
Norepinephrinefight or flight responseadrenal medulla
GABAinhibits CNSbrain
Glutamategenerally an excitatory neurotransmitter, memoryCNS, PNS

Electrical Synapse

While electrical synapses are fewer in number than chemical synapses, they are found in all nervous systems and play important and unique roles. The mode of neurotransmission in electrical synapses is quite different from that in chemical synapses. In an electrical synapse, the presynaptic and postsynaptic membranes are very close together and are actually physically connected by channel proteins forming gap junctions. Gap junctions allow current to pass directly from one cell to the next. In addition to the ions that carry this current, other molecules, such as ATP, can diffuse through the large gap junction pores.

There are key differences between chemical and electrical synapses. Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is unidirectional. Signaling in electrical synapses, in contrast, is virtually instantaneous (which is important for synapses involved in key reflexes), and some electrical synapses are bidirectional. Electrical synapses are also more reliable as they are less likely to be blocked, and they are important for synchronizing the electrical activity of a group of neurons. For example, electrical synapses in the thalamus are thought to regulate slow-wave sleep, and disruption of these synapses can cause seizures.

Nervous System, Organization of

VIII.A.1. Electrical Synapses

Electrical synapses are gap junctions. When present between neurons, they are very different from chemical synapses where the separateness of the cells is not in question. They allow the direct spread of current from one cell to another, without delay or need for receptor and decoding systems. But the individuality of the coupled cells is partly lost, and hence their utility is diminished for large nervous systems with labeled lines like those of mammals. Electrical synapses are common in invertebrate and nonmammalian nervous systems but infrequent in mammals except between neuroglial cells, where they offer the chief mode of communication. Yet they have been found between mammalian neurons and shown to transmit in a few cases. In the embryonic CNS, they are seen in many places, even in the cerebral cortex, but decline in number as chemical synapses develop. In the adult, they are usually found in cell clusters that fire action potentials synchronously, as in the lateral vestibular nucleus, which effects a rapid increase in ipsilateral extensor tone for postural maintenance, or clusters that spread influences widely, like the horizontal cells of the retina. Studies show that electrical synapses can be modulated, that they may have mechanisms favoring unidirectional conduction, and that electrical and chemical synapses have important reciprocal influences.

Paracrine Signaling

Figure 2. The distance between the presynaptic cell and the postsynaptic cell—called the synaptic gap—is very small and allows for rapid diffusion of the neurotransmitter. Enzymes in the synaptic cleft degrade some types of neurotransmitters to terminate the signal.

Signals that act locally between cells that are close together are called paracrine signals. Paracrine signals move by diffusion through the extracellular matrix. These types of signals usually elicit quick responses that last only a short amount of time. In order to keep the response localized, paracrine ligand molecules are normally quickly degraded by enzymes or removed by neighboring cells. Removing the signals will reestablish the concentration gradient for the signal, allowing them to quickly diffuse through the intracellular space if released again.

One example of paracrine signaling is the transfer of signals across synapses between nerve cells. A nerve cell consists of a cell body, several short, branched extensions called dendrites that receive stimuli, and a long extension called an axon, which transmits signals to other nerve cells or muscle cells. The junction between nerve cells where signal transmission occurs is called a synapse. A synaptic signal is a chemical signal that travels between nerve cells. Signals within the nerve cells are propagated by fast-moving electrical impulses. When these impulses reach the end of the axon, the signal continues on to a dendrite of the next cell by the release of chemical ligands called neurotransmitters by the presynaptic cell (the cell emitting the signal). The neurotransmitters are transported across the very small distances between nerve cells, which are called chemical synapses (Figure 2). The small distance between nerve cells allows the signal to travel quickly this enables an immediate response, such as, Take your hand off the stove!

When the neurotransmitter binds the receptor on the surface of the postsynaptic cell, the electrochemical potential of the target cell changes, and the next electrical impulse is launched. The neurotransmitters that are released into the chemical synapse are degraded quickly or get reabsorbed by the presynaptic cell so that the recipient nerve cell can recover quickly and be prepared to respond rapidly to the next synaptic signal.


Electrical synapses are prevalent across many brain regions, including thalamus, hypothalamus, cerebellum, and the neocortex [1–3]. In contrast to neurotransmitter-based synapses, electrical synapses are a mode of intracellular communication that transmits signals almost instantaneously, and without inactivating. Because signals cross two cell membranes, the net effect of an electrical synapse is that of a lowpass filter [3–5]: spikes are heavily attenuated, while longer or slower events, such as bursts, subthreshold rhythms, and the depolarizations that lead to spikes, are more readily shared between cells. Further, because the signal delivered is proportional to the signed difference between membrane potentials of coupled neurons, electrical synapses can exert either inhibitory or excitatory effects on a coupled neighbor, by increasing leak at rest or by transmitting activity such as post-spike hyperpolarizations, depolarizations or spikelets in either direction. A growing body of work has demonstrated ways in which electrical synapses can be modulated or modified by either synaptic [6–11] or spiking [12, 13] forms of neuronal activity.

The roles of electrical synapses in neuronal signal processing have mainly been explored in terms of their contributions to or regulation of synchrony of ongoing oscillations [14–20]. Studies focusing on the influence of electrical synapses on transient signals as they traverse the brain are fewer, but hint at specific and potentially powerful roles. For instance, propagation of spike afterhyperpolarizations through electrical synapses acts to reset and desynchronize regular firing in coupled cerebellar Golgi neurons [21]. Electrical synapses accelerate timing of spikes elicited near threshold in coupled thalamic reticular neighbors by tens of milliseconds [22, 23]. In coupled cerebellar basket cells, electrical synapses enhance and accelerate recruitment for coincident or sequential inputs [24]. Axonal gap junctions between neurons in the fly visual stream aid efficient encoding of the axis of rotation [25]. Our previous work focused on the impact of electrical synapses on transient signals in the thalamacortical relay circuit, showing that electrical coupling between inhibitory neurons leads to increased separation of disparately-timed inputs while facilitating fusion of closely-timed inputs [26].

In order to generalize a role for electrical synapses and variations in their strength in neuronal information processing, here we considered the canonical microcircuit, wherein two principal neurons, connected by an excitatory synapse, are also connected by disynaptic feedforward inhibition (Fig 1A1)[27]. This circuit motif reappears through the brain in areas ranging from the hippocampal CA1 pyramidal neurons [28], somatosensory L4 cortical neurons receiving inputs from the ventrobasal complex [29], and the cortical translaminar inhibitory circuits [30] (Fig 1A2-4). Starting with a canonical circuit, we progressively expanded models and analysis from a single circuit to a network composed of canonical circuits. We provided these models with closely timed inputs, in order to determine how the embedded electrical and inhibitory synaptic connections between interneurons influence subthreshold integration and spiking statistics at the output stage of the model. Our simulations demonstrate that electrical synapses enable a high degree of specificity and diversity of processing of transient signals for both subthreshold activity and network activity. Because electrical synapses are widespread throughout the mammalian brain, we expect that these are principles that apply widely to neuronal processing of newly incoming information as it passes through the brain.

A: The Three-cell circuit model used herein (A1) with feedforward disynaptic inhibition between excitatory source (Src) and target (Tgt) neurons. This canonical model represents those found in, for example (A2) the hippocampal circuit, between dentate gyrus (DG) and CA1 cells [28] (A3) from thalamic VB relay neurons to regular spiking cells in the somatosensory thalamocortical circuit [29] and (A4) the cortical translaminar inhibitory circuit [30]. B: Example compound subthreshold postsynaptic membrane potential (PSP) in the Tgt neuron following a spike in Src, and the quantifications (PSP peak, integration window, and area under the PSP curve (AUC)) used throughout the text. C: Effect of different inhibitory strengths GGABA→Tgt on the compound PSP in Tgt GAMPA→Tgt was 3 nS. D: Effect of varied GAMPA→Tgt on the compound PSP of Tgt GGABA→Tgt was 6 nS. For both C and D, scale bar is 1 mV, 5 ms the vertical straight line and dashed line mark the spike times of Src and Int, respectively. E-G: Combined effects of both excitatory and inhibitory synaptic strengths towards the peak, duration of the integration window and AUC of the positive portion of the compound PSP in Tgt.

Synapses: how neurons communicate with each other

Neurons talk to each other across synapses. When an action potential reaches the presynaptic terminal, it causes neurotransmitter to be released from the neuron into the synaptic cleft, a 20–40nm gap between the presynaptic axon terminal and the postsynaptic dendrite (often a spine).

After travelling across the synaptic cleft, the transmitter will attach to neurotransmitter receptors on the postsynaptic side, and depending on the neurotransmitter released (which is dependent on the type of neuron releasing it), particular positive (e.g. Na + , K + , Ca + ) or negative ions (e.g. Cl - ) will travel through channels that span the membrane.

Synapses can be thought of as converting an electrical signal (the action potential) into a chemical signal in the form of neurotransmitter release, and then, upon binding of the transmitter to the postsynaptic receptor, switching the signal back again into an electrical form, as charged ions flow into or out of the postsynaptic neuron.

An action potential, or spike, causes neurotransmitters to be released across the synaptic cleft, causing an electrical signal in the postsynaptic neuron. (Image: By Thomas Splettstoesser / CC BY-SA 4.0)

Describe the structure and function of a chemical synapse.

A synapse acts as a junction between cells - either between neurons, or between a neuron and a muscle or gland cell.

Although neurons transmit information via electrical signals, synapses transmit information rapidly via chemicals - these are called neurotransmitters.

When an action potential reaches the end of a neuron (called the pre-synaptic neuron) - called the axon terminus - the change in potential across the cell's plasma membrane stimulates the opening of voltage-gated calcium (Ca 2+ ) channels - causing calcium to rush into the axon terminus.

This in turn triggers the fusion of synaptic vesicles, which carry the molecules of neurotransmitter, with the plasma cell membrane - this releases the neurotransmitter into the gap (called the synaptic cleft) via exocytosis (the fancy word for transporting 'stuff' such as proteins out of a cell).

The neurotransmitter molecules with then travel across the gap and bind to receptors on the plasma membrane of the post-synaptic cell. This binding then triggers the influx of ions - normally sodium (Na + ) into the post-synaptic cell. If this amount of sodium reaches the threshold potential of the neuron, an action potential will be set up in this cell.

Key neurotransmitters

The first neurotransmitter to be discovered was a small molecule called acetylcholine. It plays a major role in the peripheral nervous system, where it is released by motor neurons and neurons of the autonomic nervous system. It also plays an important role in the central nervous system in maintaining cognitive function. Damage to the cholinergic neurons of the CNS is associated with Alzheimer disease.

Glutamate is the primary excitatory transmitter in the central nervous system. Conversely, a major inhibitory transmitter is its derivative γ-aminobutyric acid (GABA), while another inhibitory neurotransmitter is the amino acid called glycine, which is mainly found in the spinal cord.

Many neuromodulators, such as dopamine, are monoamines. There are several dopamine pathways in the brain, and this neurotransmitter is involved in many functions, including motor control, reward and reinforcement, and motivation.

Noradrenaline (or norepinephrine) is another monoamine, and is the primary neurotransmitter in the sympathetic nervous system where it works on the activity of various organs in the body to control blood pressure, heart rate, liver function and many other functions.

Neurons that use serotonin (another monoamine) project to various parts of the nervous system. As a result, serotonin is involved in functions such as sleep, memory, appetite, mood and others. It is also produced in the gastrointestinal tract in response to food.

Histamine, the last of the major monoamines, plays a role in metabolism, temperature control, regulating various hormones, and controlling the sleep-wake cycle, amongst other functions.

Structure of Neuron

Although different types of neurons are present in the brain, the basic structure of all the neurons is always the same. In this section, we will talk about the basic structure of neurons found in the brain.

A neuron can be divided into three basic parts cell body or perikaryon, axons, and dendrites.

Cell Body

The cell body of a neuron serves as the synthetic or trophic center for the entire cell. It is the region that contains the nucleus and the surrounding cytoplasm. The major organelles are also present in the cell body or perikaryon. These include the Golgi apparatus and the endoplasmic reticulum.

A brief detail of the major organelles found in the cell body is as follows.


The nucleus occupies is present in the central portion of the cell body of neurons. Most neurons have a large spherical central nucleus having a prominent nucleolus. In most of the cells, the nucleus is pale-staining that indicates the euchromatic nature of chromatin. The fine chromatin threads can also be visualized within the nucleus.

Rough Endoplasmic Reticulum

The cell body of the neurons is responsible for protein synthesis. It has a highly developed system of rough endoplasmic reticulum for making proteins. A large number of parallel cisternae of the reticulum are present close to the nucleus associated with polyribosomes (a group of ribosomes attached to a single copy of mRNA). They can make multiple copies of a polypeptide at the same time.

The cell body appears to be highly basophilic in the regions containing rough endoplasmic reticulum and associated polyribosomes. They are present in the form of clumps of basophilic material known as Nissl substance or Nissl bodies .

Golgi Apparatus

Recall that the Golgi apparatus is responsible for the packaging of the proteins. In the cell body of neurons, they are present adjacent to the Nissl bodies. They pack the proteins made by this system of the rough endoplasmic reticulum.

The Golgi apparatus can pack proteins in vacuoles to be transported to other organelles within the neuron or the extracellular fluid. The Golgi apparatus is exclusive to the cell body and is not found in other parts of neurons.


Mitochondria serve as the powerhouse of neurons. They are responsible for the synthesis of ATP. ATP is needed for the conduction of nerve impulses as well as other cellular processes such as intracellular transport. Mitochondria are found abundantly in the cell body of neurons. They are also present in dendrites and axons of the neuronal cell.


The cytoskeletal framework provides structural support to the cell body as well as cellular processes of neurons. This framework is made up of intermediate filaments and microtubules. The intermediate filaments found in the neurons are called neurofilaments . The filament can be viewed under a light microscope as thin threads upon silver staining after treatment with some fixatives.

The cytoskeleton not only maintains shape but is also responsible for intracellular transport of various substances.

Inclusion Bodies

Inclusion bodies are the residual bodies left in the cell body after lysosomal degradation. These appear as pigmented bodies within the cell body when viewed under a light microscope. These bodies are not harmful as they do not interfere with the cellular functions of neurons.


These are the cellular processes that carry nerve impulses towards the cell body of neurons. They function as an antenna of the neuron as they receive neuronal signals and transmit them to the cell body of a neuron.

Dendrites show abundant branching. They do not have a constant diameter. The diameter goes on decreasing as they divide into more and more branches.

The arborization pattern of dendrites is specific for different types of neurons. Tree-like arborization of dendrites is seen in most of the inter-neurons found in the brain.

Dendritic spines are small blunt processes that emerge from dendrites at specific points. These spines are the sites for synapse formation.

The cytoplasm of dendrites has the same composition as the cytoplasm found in the cell bodies of neurons. However, the cytoplasm of dendrites has abundant cytoskeletal components.


These are the cellular processes that carry nerve impulses away from the cell body of neurons. These are the cylindrical processes having a constant diameter throughout their length. In the case of the motor neurons present in the brain, they can be as long as one meter.

Axons originate from the cell body via a pyramid-shaped structure called the axon hillock. The portion of axon just beyond the axon hillock is called the initial segment. It is where the nerve impulses coming to the cell body are processed and a decision is made whether to conduct the impulse of not.

The cytoplasm present in the axons is called axoplasm. It is abundant in mitochondria and cytoskeletal filaments. However, ribosomes and RER are absent. Thus, it depends on the cell body for protein synthesis. The synaptic vesicles containing neurotransmitters are also abundantly present in the axoplasm of neurons. These vesicles are made in the cell body are then transported to the axon.

Axons do not show branching as seen in dendrites. However, the terminal end of axons, called the axon terminal, forms multiple branches called terminal arborization.

3. The Chemical Synapse and Neurotransmitters

Neurons are not in direct physical contact with each other, but instead come into very close proximity at a structure called the synapse. The neuron sending a signal to the next is called the presynaptic neuron, and the neuron receiving a signal is called the postsynaptic neuron, shown here:

Chemical transmission involves release of chemical messengers known as neurotransmitters. Neurotransmitters carry information from the pre-synaptic (sending) neuron to the post-synaptic (receiving) cell. Image credit: Khan Academy

There is a small gap between the two neurons called the synaptic cleft, where neurotransmitters are released by the presynaptic neuron to transmit the signal to the postsynaptic neuron, shown here:

Inside the axon terminal of a sending cell are many synaptic vesicles. These are membrane-bound spheres filled with neurotransmitter molecules. There is a small gap between the axon terminal of the presynaptic neuron and the membrane of the postsynaptic cell, and this gap is called the synaptic cleft. Image credit: Khan Academy

How does synaptic transmission work? Once the action potential reaches the end of the axon, it propagates into the pre-synaptic terminal where the following events occur in sequence:

  1. The action potential depolarizes the membrane and opens voltage-gated Na + channels. Na + ions enter the cell, further depolarizing the presynaptic membrane.
  2. This depolarization causes voltage-gated Ca 2+ (calcium) channels to open in the presynaptic neuron, allowing calcium ions to enter the presynaptic neuron at the synpase.
  3. Calcium ions entering the presynaptic neuron cell initiate a signaling cascade that causes small membrane-bound vesicles, called synaptic vesicles, to fuse with the presynaptic membrane. The synaptic vesicles contain neurotransmitter molecules.
  4. Fusion of a vesicle with the presynaptic membrane causes neurotransmitter to be released into the synaptic cleft , the extracellular space between the presynaptic and postsynaptic membranes. The neurotransmitter diffuses across the synaptic cleft and binds to receptor proteins on the postsynaptic membrane.

This process is illustrated below:

Communication at chemical synapses requires release of neurotransmitters. When the presynaptic 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 in the postsynaptic membrane, resulting in a localized depolarization or hyperpolarization of the postsynaptic neuron. Image credit: Khan Academy

  • Excitatory postsynaptic potentials (EPSPs) make a postsynaptic neuron more likely to fire an action potential. For example, when acetylcholine is released at the synapse between a nerve and muscle (called the neuromuscular junction) by a presynaptic neuron, it causes postsynaptic Na + channels to open. Na + enters the postsynaptic cell and causes the postsynaptic membrane to depolarize.
  • Inhibitory postsynaptic potentials (IPSPs) make a postsynaptic neuron less likely to fire an action potential. For example, when the neurotransmitter GABA (gamma-aminobutyric acid) is released from a presynaptic neuron, it binds to and opens Cl – channels. Cl – ions enter the cell and hyperpolarizes the membrane.

Once neurotransmission has occurred, the neurotransmitter must be removed from the synaptic cleft so the postsynaptic membrane can “reset” and be ready to receive another signal. This can be accomplished in three ways:

  • the neurotransmitter can diffuse away from the synaptic cleft
  • the neurotransmitter can be degraded by enzymes in the synaptic cleft
  • the neurotransmitter can be recycled (sometimes called reuptake) by the presynaptic neuron.

This video walks through the process of signal communication across a chemical synapse:

While action potentials are “all-or-nothing,” as noted above, EPSPs and IPSPs are graded they vary in magnitude of depolarization or hyperpolarization, as illustrated below:

Graded potentials are temporary changes in the membrane voltage, the characteristics of which depend on the size of the stimulus. Some types of stimuli cause depolarization of the membrane, whereas others cause hyperpolarization. It depends on the specific ion channels that are activated in the cell membrane. Image credit: OpenStax Anatomy & Physiology

Often a single EPSP is not strong enough to induce an action potential in the postsynaptic neuron on its own, and multiple presynaptic inputs must create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential. This process is called summation and occurs at the axon hillock, as illustrated below. In addition, each neuron often has inputs from many presynaptic neuron – some excitatory and some inhibitory – so IPSPs can cancel out EPSPs and vice versa. It is the net change in postsynaptic membrane voltage that determines whether the postsynaptic cell has reached its threshold of excitation needed to fire an action potential. Together, synaptic summation and the threshold for excitation act as a filter so that random “noise” in the system is not transmitted as important information.

A single neuron can receive both excitatory and inhibitory inputs from multiple neurons, resulting in local membrane depolarization (EPSP input) and hyperpolarization (IPSP input). 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. Image credit: OpenStax Biology

This video, added after the IKE was opened, provides an overview of summation in time and space:

Here are two final videos to help you put this all together (in a more engaging way than any of the videos above). Note that these videos do not provide any new information, but they may help you better integrate all the information previously discussed: