Synapses - The Connection of Our Nerves

At the end of the axon of a neuron, the action potential reaches the synapse.

The synapse (end button) consists of the presynaptic membrane (at the end of the axon), the synaptic cleft (filled with extracellular fluid), and the postsynaptic membrane (e.g., dendrite, muscle cell).

It forms the contact point with another neuron (dendrite), a muscle or gland cell/organ.

The synapse thus represents a connection between two excitable cells. It converts electrical impulses (from the nerve cell) into a chemical messenger (neurotransmitter), which in turn results in an electrical stimulus and either inhibits or depolarizes the postsynaptic cell!

Chemical synapse schema cropped, marked as public domain, details on Wikimedia Commons

Synapses – Electrical Signal Transmission, Chemical Transfer

The action potential is transmitted from the cell body through the axon, which, as we know, can be very long. The better the axon is insulated, the faster this impulse transmission functions, or even works over long distances.

We have differently thick myelinated nerves and consequently different impulse conduction velocities (better insulated is faster). This has advantages, as we will see later/in another blog!

The electric action potential thus triggers a release of neurotransmitter in the synapse in combination with Ca+, which are already packed and ready in vesicles. These neurotransmitters diffuse through the synaptic cleft, where they then trigger an action again, e.g., another depolarization of a neuron or a muscle cell (with subsequent muscle contraction).

anonymous, Chem. Synapse scheme, marked as public domain, details on Wikimedia Commons

A neuron specializes in a specific function and thus on certain neurotransmitters! It, therefore, primarily has a specific neurotransmitter that can trigger something. The neurotransmitters are specific to certain receptors, this is referred to as a lock-and-key function.

These neurotransmitters are divided into excitatory or inhibitory substances, where excitatory ones lead to signal transmission (e.g., acetylcholine in motor transmission), while inhibitory ones lead to non-transmission with corresponding signal blocking and shutdown.

Inhibitory neurotransmitters affect the conductivity of K+ channels on the postsynaptic membrane (see our blog on action potentials): Due to the K+ efflux (outflow from the cell interior), the already negative cell interior becomes even more negative, and the membrane becomes hyperpolarized! In this state, no further immediate excitation by impulses is possible! This is then referred to as an inhibitory postsynaptic potential (IPSP, inhibiting from -70 to -100mV). At this moment, and in this state, the membrane is not excitable!

Savant-fou, Synapse neuro-neuronal, CC BY-SA 3.0

Production of Neurotransmitters

Neurotransmitters like acetylcholine (transmitter in motor transmission) are produced in the cell body (here from choline and acetyl). Acetyl is a substance produced in the citric acid cycle, a cycle for energy production in combination with oxygen within our mitochondria. And thanks to this constant production, it is available in abundant supply. Choline, however, is not available to the body in such large quantities.

The finished neurotransmitters are packaged in granules or vesicles (small bubbles) and are also transported to the synapses in the axon, where they are stored ready for release.

After release into the synaptic cleft, the neurotransmitters are quickly split back into their previous components by specific enzymes (for example, with acetylcholine by acetylcholinesterase). The breakdown products are either washed away by the bloodstream (e.g., acetyl), or (like choline, which is not as widespread as acetyl) absorbed back into the synapse. From these, after their return to the cell nucleus, new neurotransmitters are synthesized again.

A quick breakdown of released and active neurotransmitters is beneficial: Action potentials often occur in quick succession (1-2 ms, as we have seen in our previous blog), and these signals should be transmitted.

Otherwise, a constant effect of acetylcholine on a muscle cell would result in prolonged contraction.

Diseases and Pathologies

It is also important to know that these neurotransmitters, like all substances, are produced in the cell body of the nerve cell itself. The entire axon is also supplied with its own vessels and lines from the cell nucleus. This also means that they need to be transported the long distance from the cell body to the synapse!

This is where a problem lies in various pathologies: For instance, if there is pressure (from a herniated disc) on the cell body of a motor neuron, which lies in the spinal cord, the production of these neurotransmitters is disrupted. Paralysis symptoms can occur.

If a structure rather puts pressure on the axon, the blood supply of the axon (including the axonal transport of transmitters packed in vesicles) is disrupted. This can lead to pain and paresthesias, or in the case of greater pressure, also lead to motor failures.

This helps to understand why pressure on an axon might be very painful, but not always as dramatic as pressure directly on the cell nucleus: if the cell nucleus dies (which can happen in a relatively short time and is a medical emergency), the entire neuron fails. However, as long as the necessary substances and building blocks can be produced in the cell nucleus, there is also a possibility of regeneration and recovery of neuronal structures.

Poisoning and Effects of Poisons

Another issue is competitive inhibition by other substances: Competitive because there are molecules that fit better in terms of structure and form (higher affinity) to the receptor than the neurotransmitter! This substance, however, has no effect, but occupies the receptor, so the transmitter cannot dock and thus no reaction is triggered!

This happens, for example, in carbon monoxide (CO) poisoning (smoke inhalation poisoning): the gas binds much better to hemoglobin (higher affinity) than oxygen. This consequently interrupts this oxygen transport through the blood, with potentially fatal consequences.

This possibility of competitive inhibition is also often used in insecticides so that neurotransmitters can no longer dock.

Another possibility is an inhibitory effect on acetylcholinesterase (the splitting enzyme for acetylcholine), as in the case of the nerve gas sarin. This results in prolonged contraction of the muscles, which, due to the effects on our respiratory system, can have fatal consequences.

Training and Rehabilitation

Synapses are also highly adaptable: More synapses can be built on one hand, and on the other hand, more receptors can be incorporated into the postsynaptic membrane. This represents two possibilities or mechanisms for a modification/sensitization of the signal, with receptors in particular being able to be incorporated into a membrane relatively quickly.

Postsynaptic density, Katharina Heupel et al, Postsynaptic density, CC BY 2.0

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Savant-fou, Synapse neuro-neuronal, CC BY-SA 3.0