Video: Neuronal synapses

Have you ever wondered how the billions of neurons across your entire body communicate with each other? Imagine your nervous system is a vast archipelago -- a system of islands connected by an intricate network of bridges. Each island represents a neuron, bustling with activity and information. But how does all this vital information travel from one island to another?

That's where our neural bridges come in -- structures known as neuronal synapses. These microscopic bridges are the vital links that allow signals to hop from one neuronal island to the next. Without them, each neuron would be isolated, unable to share its information with the neurons around it.

Let's see exactly how these neuronal synapses get the job done.

A synapse is a junction between two cells which serves as the primary site of communication between a presynaptic neuron, transmitting the signal, and a postsynaptic cell, receiving the signal. Synapses aren't only found between two neurons, but also between a neuron and an effector cell, like a muscle cell or gland. However, not all neuronal synapses transmit a signal in the same way.

Let's take a closer look at two distinct variations of the neuronal synapse: the vesicular, or chemical, synapse and the nonvesicular, or electrical, synapse.

First up, let's briefly meet the speed demons of neural communication -- the nonvesicular synapse, commonly referred to as an electrical synapse, where information zips directly from one neuron to another. Here's the quick lowdown.

They use gap junctions, which are unique, protein-based channels that create direct physical links or bridges between the presynaptic and postsynaptic membranes of synapsing neurons. They allow ion currents and small to medium signaling molecules to passively and rapidly flow through the gap junction channels, which subsequently allows changes in membrane potential in the presynaptic neuron to directly trigger an almost instantaneous corresponding change in the postsynaptic neuron.

They're predominantly bidirectional, meaning the information can flow both ways. You'll find these types of synapses where split-second timing is crucial, like the retina of the eye, where horizontal cells and amacrine cells utilize electrical synapses to synchronize their activity, facilitating rapid and coordinated visual processing for functions such as contrast enhancement and motion detection.

Now let's take a look at the more common type of neuronal synapse -- the vesicular, or chemical, synapse. As with all synapses, it involves a presynaptic neuron and a postsynaptic cell which, in this example, is another neuron. The presynaptic terminal, also known as the terminal bouton, is packed with membrane-bound spheres called synaptic vesicles, which are filled with different types of neurotransmitters.

These can be either excitatory, inhibitory, or modulatory, which is based on their effect on the postsynaptic neuron. For example, excitatory neurotransmitters like glutamate make it more likely for an action potential to continue while inhibitory neurotransmitters like GABA makes it less likely.

The part of the presynaptic terminal which faces the postsynaptic terminal is known as the presynaptic membrane. Within the region, there's specialized areas called the active zone. This is where synaptic vesicles dock and fuse with the presynaptic membrane to release neurotransmitters. It is composed of a protein complex that works to organize neurotransmitter release and is crucial for both the speed and precision of synaptic transmission as well as for various forms of synaptic plasticity.

As an action potential arrives at the presynaptic terminal carried by the sequential opening of voltage-gated sodium ion channels, it activates voltage-gated calcium ion channels, allowing the influx of calcium ions into the cell. This causes the neurotransmitter-containing vesicles to fuse with the presynaptic membrane and neurotransmitters are released into the synaptic cleft via exocytosis. The more frequent the action potential is arriving at the terminal bouton, the more neurotransmitter that is released.

The synaptic cleft is a gap between the presynaptic and postsynaptic membranes. It's really thin, only about 20 to 50 nanometers wide, and is the space into which the synaptic vesicles dump their neurotransmitters as they move between neurons.

The postsynaptic terminal has a postsynaptic membrane dotted with neural receptors that are like tiny catchers' mitts, ready to grab the neurotransmitters. When a neurotransmitter binds to its receptor on the postsynaptic membrane, it can cause all sorts of excitement or inhibition in the postsynaptic neuron.

There are two main types of receptors: ionotropic receptors and metabotropic receptors.

Ionotropic receptors are ligand-gated ion channels that open directly in response to neurotransmitter binding. They produce fast, short-lived responses by allowing ions to flow directly into the cell. Metabotropic receptors work through what's known as G-protein-coupled cascades. When activated, they trigger a series of intracellular events that can lead to long-lasting and more diverse effects on the cell.

It's like a molecular key fitting into a lock, triggering either a quick opening of a gate -- ionotropic -- or setting off a complex chain reaction – metabotropic. Both types can significantly change the neuron's behavior, but on different timescales and through different mechanisms.

Neurotransmitters remaining in the synaptic cleft which do not bind with receptors on the postsynaptic membrane are then either reabsorbed by the presynaptic neuron or nearby glial cells which is called reuptake, or broken down by enzymes which terminates the neurotransmitter activity. It's always a one-way street, though; information flows from the presynaptic to the postsynaptic neuron, not the other way around.

All right, neuroscientists, time for a quick recap. Let's make sure we really understand this process by following a synaptic transmission as it would happen chronologically.

First, the action potential arrives at the presynaptic terminal via the sequential opening of voltage-gated sodium ion channels, which causes the presynaptic membrane to depolarize. This then triggers voltage-gated calcium ion channels to open. Then calcium ions rush into the presynaptic terminal which causes synaptic vesicles to fuse with the presynaptic membrane. The vesicles release their cargo of neurotransmitters into the synaptic cleft through exocytosis where they can diffuse across the open space and bind to specific receptors on the postsynaptic membrane.

Depending on the neurotransmitter and receptor type, the neurotransmitters will cause ion channels to open which brings about changes in the membrane potential in this region of the postsynaptic membrane. Excess neurotransmitters are either reclaimed by the presynaptic neuron through a process called reuptake, or they are decomposed by specific enzymes in the synaptic cleft.

Great! Now that we understand the process of synaptic transmission, let's talk about what happens next -- the postsynaptic potentials.

These are the changes in membrane potential that happens in the postsynaptic membrane after neurotransmitters bind to their receptors. We've got two types here: excitatory postsynaptic potentials, or EPSPs, and inhibitory postsynaptic potentials, or IPSPs. Let's break it down.

First up, excitatory postsynaptic potentials, or EPSPs. These occur when a neurotransmitter activates ion channels on the postsynaptic membrane specific for positively charged ion channels like sodium or calcium. The influx of positively charged ions makes the postsynaptic neuron more likely to fire an action potential by slightly depolarizing the membrane, making the membrane potential less negative and closer to the threshold potential for an action potential to trigger. Excitatory postsynaptic potentials are often triggered by excitatory neurotransmitters like glutamate.

Now for the inhibitory postsynaptic potentials, or IPSPs. These make the postsynaptic neuron less likely to fire an action potential by hyperpolarizing the membrane or preventing depolarization. This occurs through two primary mechanisms. First, the neurotransmitter causes ion channels to open which allow negatively charged ions like chloride to enter the postsynaptic neuron. Or alternatively, the neurotransmitter causes potassium ion channels to open, allowing positively charged potassium ions to leave the postsynaptic neuron.

Either way, the addition of negatively charged ions or loss of positively charged ions from the intracellular environment causes the postsynaptic membrane potential to become more negative, moving further from the threshold potential. Inhibitory postsynaptic potentials are typically caused by neurotransmitters like GABA which binds to GABA-A chloride channels or GABA-B potassium receptors.

Whether a synapse is excitatory or inhibitory doesn't depend solely on the neurotransmitter but on the specific receptors present and the ions they allow to pass. The same neurotransmitter can have different effects depending on the receptor type and the cell's internal ion concentrations.

Now, here's where things get really exciting. You see neurons are constantly receiving multiple inputs from different synapses or receiving repeated input from the same neuron in a short period of time and they need to decide whether to fire an action potential or not. That's where something called summation comes in.

We've got two types: temporal and spatial summation.

Let's first take a look at temporal summation. This is when multiple signals are received from a single presynaptic neuron in quick succession. If they arrive fast enough, their effects cumulatively bring the membrane potential at the trigger zone closer and closer to the threshold potential. Since excitatory postsynaptic potentials are very short-lived, they must occur in very rapid succession in order for temporal summation to work; otherwise, the threshold potential will not be reached.

Now let's take a look at spatial summation. This occurs when signals arrive at different synapses on the neuron at about the same time. Collectively, they bring about a surge in membrane potential, bringing it to threshold and triggering an action potential.

Both types of summation can involve excitatory and inhibitory postsynaptic potentials. For example, during sensory adaptation, a neuron might initially respond to a continuous touch stimulus with excitatory postsynaptic potentials, bringing its membrane potential closer to the threshold for an action potential. Over time, inhibitory interneurons generate inhibitory postsynaptic potentials that hyperpolarize the cell membrane, counteracting the excitatory postsynaptic potentials, and making it harder to reach the threshold.

Both types of summation can involve excitatory and inhibitory postsynaptic potentials. This summation is crucial for information processing in the brain. It allows neurons to integrate information from multiple sources and make complex decisions.

And that wraps up our synaptic adventure for today. We've journeyed through the microscopic world of synapses, from their structure to their function, and from chemical messengers to postsynaptic potentials. We've seen how these tiny communication hubs form the backbone of your nervous system's information highway.

To cement your synaptic knowledge, why not check out our quiz and other learning materials in our study unit on neuronal synapses. It's a great way to strengthen those neural connections we just talked about.

See you next time.