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Young Minds. Author manuscript; available in PMC 2020 Dec 9. Published in final edited form as: PMCID: PMC7725213 NIHMSID: NIHMS1642668 In biology, electricity is the flow of charged particles [ions] moving across the surface layer of a cell, which is called a membrane
[1]. The movement of ions carries an electrical wave along the length of a nerve cell, which is called a neuron. The neuron has local branches [like a tree] that receive signals, which are called dendrites, and a longer, simpler projection [like a tree trunk] that sends signals, which is called an axon
[Fig. 1]. How does the electrical signal jump from one neuron to another? Near the end of the axon, there are special communication junctions called synapses [Fig. 1]. A
synapse releases chemical signals, which are called neurotransmitters. These signals travel to another neuron to create a new electrical wave in that cell.HOW DO NEURONS SEND AND RECEIVE MESSAGES?
Communication between two nerve cells
The structure of a nerve cell, and the site of cell-to-cell communication [the “synapse”].
How does an electrical wave travel down a neuron? The cell membrane contains gated protein channels that can open and shut, to allow ions to enter or leave the cell [permeability] [1]; like the automatic sliding doors at the grocery store. When such a channel opens, it lets ions flood into the cell, carrying electrical charge [Fig. 2]. This causes the next channel along to open, and then the next, such that the electrical wave moves along the cell. To return to rest, a different channel opens more slowly to allow the ions to leave the cell [1]. This ends the electrical wave, setting the stage for the next electrical wave to start the cycle again. The movement of ions continues along the axon to reach synapses near the axon terminus [Fig. 2].
Communication at the synapse
Synapses work the same way. The electron microscope picture shows a neuromuscular junction.
HOW DOES A SYNAPSE WORK TO COMMUNICATE BETWEEN CELLS?
The electrical wave causes the neuron to release small chemical neurotransmitters at the synapse [1], which then travel across to the other cell to attach to proteins on the cell surface, which is called a membrane [Fig. 2]. These proteins are called receptors. Neurotransmitters are packaged inside little round spheres called vesicles, which can fuse with the outside membrane to release the signal [Fig. 2]. When these vesicles fuse with the cell membrane, they release the chemicals outside of the cell [Fig. 2]. These chemicals then move through the space between the sender cell and the receiver cell [1]. This happens very quickly because the space is very, very narrow [Fig. 2]. When the chemical neurotransmitter reaches the receiver cell, it binds to special receptors in that membrane, which causes new channels to open [Fig. 2]. Ions flow into the receiver cell and this creates a new electrical message [2].
This is also how our neurons communicate with our muscles, telling us when to move. The special movement synapse is called the neuromuscular junction [Fig. 2] [3]. In people, the neurotransmitter here is acetylcholine, and the muscle receptor is the acetylcholine receptor. Just like in neurons, the binding of the neurotransmitter causes receptors to open as channels in the muscle, allowing ions to flood into the muscle [Fig. 2] [3]. In the muscle, this electrical message causes the muscle to contract or shorten. Think about catching a ball: your brain tells a neuron to send an electrical signal to the neuromuscular junction synapse, and this causes neurotransmitter to be released onto your finger muscles, so that they contract to catch the ball.
HOW DO SYNAPSES ALLOW ME TO SEE AND HEAR?
Our senses detect the world around us and transduce the many external forms of energy [light, sound, movement] into electrical messages in our neurons. In our eyes, for example, there are light-detecting neurons called photoreceptors that respond to the things we see [1]. Some of these special neurons detect colored light [red, green, blue] and some detect just black and white; like an old-fashioned photograph. Light causes channels to open in these different light-detecting neurons, which sends an electrical message to the synapses of neurons inside your brain [Fig. 3]. Signals travel along the optic nerve to carry information into your brain [1]. This information is then processed in visual center synapses to interpret the light images.
Many synapses communicate within our brain
More synapses form and strengthen as we learn and make memories.
For us to hear, sensory receptors in our ears are actually activated by movement, as sound is movement vibrations travelling through the air. These air vibrations move tiny hairs on our ear nerve cells [1]. This movement opens channels, allowing ions to flood into the cell and create the electrical message [Fig. 2]. As a result, neurotransmitters are released at the synapse between the hair cell and a brain neuron [Fig. 2]. How loud the sound is depends on how many hairs are bent. Greater bending causes more neurotransmitter to be released at the synapse, which then creates more electrical messages into the brain [Fig. 3]. These signals travel along the auditory nerve, which connects through synapses to brain neurons interpreting smells [1].
HOW DO SYNAPSES ALLOW ME TO LEARN AND REMEMBER?
One of the most important things about our brains is that synapses change when we use them. These changes in our synapses [plasticity] allow us to learn new information, and then remember what we have learned [2]. The number and size of synapses can change as we use them. If we use our synapses a lot, many more can form [Fig. 3]. If we do not use them as much, synapses can shrink or decrease in number [2]. The strength of communication between synapses can also change depending on how much we use them. If we use them a lot, this can increase the amount of neurotransmitter released, or neurotransmitter receptors on the receiving cell [Fig. 2] [2]. Synapses are like muscles; they are strengthened by use.
If we use our synapses a lot for a long time, synapse strengthening can also be maintained for a very long time. This process is known as long-term potentiation [2]. If we use our synapses a lot, it can create new synapses that remain in place for many years, even decades. Long-term potentiation is what happens when we form long-term memories, and what happens when we convert short-term memories into long-term memories [2]. As you know, you can remember things for years; think of your mother’s face, or your best friend in the first grade. Since your synapses are so important for moving, sensing, learning and remembering, it is easy to see how problems with synapses can cause diseases and disabilities [4–6].
WHAT HAPPENS WHEN SYNAPSES DO NOT WORK PROPERLY?
When synapses do not work properly, your brain cannot communicate within itself and with your body muscles. Movement disorders often result from problems at the neuromuscular junction [4]. Diseases result from problems in sending or receiving neuromuscular junction signals [Fig. 2]. For example, one disease is caused by the neurotransmitter acetycholine not being cleared out of the synapse. Acetylcholine is released at the neuromuscular junction synapse to cause muscles to contract [Fig. 2]. If it is not properly removed afterwards, then acetycholine will continue to bind muscle receptors [Fig. 2]. This will cause improper muscle contraction and movement, later loss of the receptors, and eventually the loss of the muscles [4].
Similarly in our senses, problems with synapses can cause a loss our sensory perception. Deafness can occur due to problems in synapses in our ear hair cells and the overactivation of auditory neurons [5]. If our hearing neurons are activated over and over again, it takes a stronger electrical message to continue to activate them. As a result, ear hair cells in people with hearing problems need to feel a louder sound in order to pass on the message to neurons in the auditory nerve [5]. This is known as an increased hearing threshold. In cases of blindness, photoreceptor synapse problems can cause photoreceptor cells to disappear completely [6]. Thus, light cannot be turned into electrical signals, and the information is not carried into the brain.
Finally, problems with the plasticity of brain synapses can cause thinking disabilities and autism [1,2]. Perhaps you know someone with autism spectrum disorder? This problem causes a state of reduced social interaction and abilities to communicate with your friends and family. One clear cause of autism is that synapses do not change as much as they should when they are used [1,2]. In this condition, new synapses do not form as well as usual and therefore communication between neurons is weakened. Although the causes of autism are still being determined, it is clear that it is related to our genes. One problem that can decrease the plasticity of synapses occurs in people with Down’s syndrome.
WHY DO WE NEED TO KNOW ABOUT SYNAPSES?
So many functions of your body are carried out based on synapse communication between cells! Right now, as you are reading this, literally trillions of synapses are sending signals whizzing around your brain and into the rest of your body. Neurons are driving movement in your muscles through neuromuscular junction synapses; allowing your eyes to move and your fingers to tap! Your brain synapses are receiving sensory information from your eyes, your ears and your other senses, and you are using this blizzard of information to make the best decisions about what you should do. Your synapses are changing to allow you to learn, and to remember what you learn. Hopefully, the information in this article will stay in your brain synapses as long-term memory!
GLOSSARY
| Ions | positive or negative charged salt particles that move through your cell membranes |
| Permeability | the number of ions moving through a cell membrane over a period of time |
| Neuromuscular junction | the special synapse between a motor neuron and a muscle cell |
| Transduce | to turn one type of energy into another type of energy; like light to electricity |
| Plasticity | the ability of all your synapses to change based on the amount you use them |
AUTHOR BIOGRAPHIES
Athira Sivadas: I am a pre-med undergraduate student at Vanderbilt University in Nashville, Tennessee. My interests lie in the molecular basis of neurological disorders, such as Autism and Down’s syndrome. I am especially interested in environmental effects on brain structure and plasticity. In my free time, I volunteer for the American Red Cross.
Kendal Broadie: I am the Stevenson Professor of Neurobiology at Vanderbilt University. I have studied synapses for more than 30 years, including synapse development [synaptogenesis], synapse function [neurotransmission], and use-dependent synapse change [synaptic plasticity]. I also model synaptic diseases, such as Autism Spectrum Disorder [ASD].
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