The Nervous System, Part 3 – Synapses!: Crash Course A&P #10

The Nervous System, Part 3 – Synapses!: Crash Course A&P #10

What’s 1000 times thinner than a piece of
paper, more numerous in you than grains of sand on a beach, and proof that the smallest
things can sometimes be the most powerful? I’m talking about the synapse — the meeting
point between two neurons. If your neurons form the structure of your
nervous system, then your synapses — the tiny communication links between them — are
what turn that structure into an actual system. Because, as great and powerful as your neurons
are, when it comes down to it, their strength and their purpose lies in their connections.
A single neuron in isolation might as well not exist if it doesn’t have someone to
listen or talk to. The word “synapse” comes from the Greek
for “to clasp or join.” It’s basically a junction or a crossroads. When an action potential — and if you don’t
know what an action potential is, watch the last episode — sends an electrical message
to the end of an axon, that message hits a synapse that then translates, or converts
it, into a different type of signal and flings it over to another neuron. These connections are rather amazing feats
of bio-electrical engineering, and they are also ridiculously, mind-bogglingly numerous. Consider that the human brain alone has 100
billion neurons, and each of those has 1000 to 10,000 synapses. So you’ve got somewhere between 100 to 1,000
trillion synapses in your brain. Each one of these hundreds of trillions of
synapses is like a tiny computer, all of its own, not only capable of running loads of
different programs simultaneously, but also able to change and adapt in response to neuron
firing patterns, and either strengthen or weaken over time, depending on how much they’re
used. Synapses are what allow you to learn and remember. They’re also the root of many psychiatric
disorders. And they’re basically why illicit drugs
— and addictions to them — exist. Pretty much everything in your experience
— from euphoria to hunger to desire to fuzziness to to confusion to boredom — is communicated
by way of these signals sent by your body’s own electrochemical messaging system. Hopefully, you know enough about email and
texting etiquette to know that if you’re gonna communicate effectively, you have to
respect the sanctity of the group list. It’s not a great idea to send a mass text
to all of your friends first thing in the morning to give them the urgent news that you
just ate a really delicious maple-bacon donut. Seriously, people. If you happen to have a friend who
truly adores bacon, then an email would suffice. But! If you’re out clubbing and suddenly
Bill Murray shows up and starts doing karaoke… then that would be a totally appropriate time
to notify all of your friends at once that something awesome is happening and they better
be a part of it. And in much the same way — OK, in kind of
the same way — your nerve cells have two main settings for communicating with each other,
depending on how fast the news needs to travel. Some of your synapses are electrical — that
would be like an immediate group text. Others are chemical synapses — they take
more time to be received and read, but they’re used more often and are much easier to control,
sending signals to only certain recipients. Fortunately, your nervous system has better
text etiquette than your mom, and knows when each kind is appropriate to use, and how to
do it. Your super fast electrical synapses send an
ion current flowing directly from the cytoplasm of one nerve cell to another, through small
windows called gap junctions. They’re super fast because the signal is
never converted from its pure electrical state to any other kind of signal, the way it is
in a chemical synapse. Instead, one cell and one synapse can trigger
thousands of other cells that can all act in synchrony. Something similar happens in
the muscle cells of your heart, where speed and team effort between cells is crucial. This seems like a good system, so why aren’t
all of our synapses electrical? It’s largely a matter of control. With such
a direct connection between cells, an action potential in one neuron will generate an action
potential in the other cells across the synapse. That’s great in places like your heart, because
you definitely don’t want a half a heartbeat. But if every synapse in your body activated
all of the neurons around it, your nervous system would basically always be in “group
text” mode, with every muscle fiber and bit of organ tissue always being stimulated
and then replying-all to the whole group which would stimulate them even more until everyone
just got maxed out and exhausted and turned off their phones for good…which would be
death. So that would be bad, which is partly why
we have chemical synapses. They are much more abundant, but also slower, and they’re more precise
and selective in what messages they send where. Rather than raw electricity, these synapses
use neurotransmitters, or chemical signals, that diffuse across a synaptic gap to deliver
their message. The main advantage chemical synapses have
over electrical ones is that they can effectively convert the signal in steps — from electrical
to chemical back to electrical — which allows for different ways to control that impulse. At the synapse, that signal can be modified,
amplified, inhibited, or split, either immediately or over longer periods of time. This set-up has two principal parts: The cell that’s sending the signal is the
presynaptic neuron, and it transmits through a knoblike structure called the presynaptic
terminal, usually the axon terminal. This terminal holds a whole bunch of tiny
synaptic vesicle sacs, each loaded with thousands of molecules of a given neurotransmitter. The receiving cell, meanwhile, is, yes, thankfully
the postsynaptic neuron, and it accepts the neurotransmitters in its receptor region, which is
usually on the dendrite or just on the cell body itself. And these two neurons communicate even though
they never actually touch. Instead, there’s a tiny gap called a synaptic cleft between them —
less than five millionths of a centimeter apart. One thing to remember is that messages that
travel via chemical synapses are technically not transmitted directly between neurons,
like they are in electrical synapses. Instead, there’s a whole chemical event
that involves the release, diffusion, and reception of neurotransmitters in order to
transmit signals. And this all happens in a specific and important
chain of events. When an action potential races along the axon
of a neuron, activating sodium and potassium channels in a wave, it eventually comes down
to the presynaptic terminal, and activates the voltage-gated calcium (Ca2+) channels
there to open and release the calcium into the neuron’s cytoplasm. This flow of positively-charged calcium ions
causes all those tiny synaptic vesicles to fuse with the cell membrane and purge their
chemical messengers. And it’s these neurotransmitters that act like couriers diffusing across the
synaptic gap, and binding to receptor sites on the postsynaptic neuron. So, the first neuron has managed to convert
the electrical signal into a chemical one. But in order for it to become an action potential
again in the receiving neuron, it has to be converted back to electrical. And that happens once a neurotransmitter binds
to a receptor. Because, that’s what causes the ion channels to open. And depending on which particular neurotransmitter
binds to which receptor, the neuron might either get excited or inhibited. The neurotransmitter
tells it what to do. Excitatory neurotransmitters depolarize the
postsynaptic neuron by making the inside of it more positive and bringing it closer to
its action potential threshold, making it more likely to fire that message on to the
next neuron. But an inhibitory neurotransmitter hyperpolarizes
the postsynaptic neuron by making the inside more negative, driving its charge down — away
from its threshold. So, not only does the message not get passed along, it’s now even
harder to excite that portion of the neuron. Keep in mind here: Any region of a single
neuron may have hundreds of synapses, each with different inhibitory or excitatory neurotransmitters.
So the likelihood of that post-synaptic neuron developing an action potential depends on the sum
of all of the excitations and inhibitions in that area. Now, we have over a hundred different kinds
of naturally-occurring neurotransmitters in our bodies that serve different functions.
They help us move around, and keep our vital organs humming along, amp us up, calm us down,
make us hungry, sleepy, or more alert, or simply just make us feel good. But neurotransmitters don’t stay bonded
to their receptors for more than a few milliseconds. After they deliver their message, they just sort of pop
back out, and then either degrade or get recycled. Some kinds diffuse back across the synapse
and are immediately re-absorbed by the sending neuron, in a process called reuptake. Others are broken down by enzymes in the synaptic
cleft, or sent away from the synapse by diffusion. And this mechanism is what many drugs — both
legal and illegal — so successfully exploit, in order to create their desired effects. These drugs can either excite or inhibit the production,
release, and reuptake of neurotransmitters. And sometimes they can simply mimic neurotransmitters,
tricking a neuron into thinking it’s getting a natural chemical signal, when really it’s
anything but. Take cocaine, for example. Don’t take cocaine. Once it hits your bloodstream, it targets
three major neurotransmitters — serotonin, dopamine, and norepinephrine. Serotonin is mainly inhibitory and plays an
important role in regulating mood, appetite, circadian rhythm, and sleep. Some antidepressants can
help stabilize moods by stabilizing serotonin levels. And when you engage in pleasurable activities
— like hugging a loved one, or having sex, or eating a really, really great donut — your
brain releases dopamine, which influences emotion and attention, but mostly just makes
you feel awesome. Finally, norepinephrine amps you up by triggering
your fight or flight response, increasing your heart rate, and priming muscles to engage, while
an undersupply of the chemical can depress a mood. So in a normal, sober state, you’ve got
all these neurotransmitters doing their thing in your body. But once they’ve delivered
their chemical payloads, they’re usually diffused right back out across the synapse
to be absorbed by the neuron that sent them. But cocaine blocks that reuptake, especially
of dopamine, allowing these powerful chemicals to float around and accumulate — making the user feel
euphoric for a time, but also paranoid and jittery. And because you have a limited supply of these
neurotransmitters, and your body needs time to brew more, flooding your synapses like
this eventually depletes your supply, making you feel terrible in a number of ways. Cocaine and other drugs that target neurotransmitters
trick the brain, and after prolonged use may eventually cause it to adapt, as all those synapses
remember how great those extra chemicals feel. As a result, you actually start to lose receptors,
so it takes even more dopamine, and finally cocaine, to function normally. Sometimes the best way to understand how your
body works is to look at how things can go wrong. And when it comes to your synapses,
that, my friends, is what wrong looks like. In their natural, healthy state, your synapses
know when to excite, when to inhibit, when to use electricity and when to dispatch the
chemical messengers. Basically, a healthy nervous system has the
etiquette of electrical messaging down to, well, a science. Today you learned how electrical synapses
use ion currents over gap junctions to transmit neurological signals, and how chemical synapses
turn electrical signals into chemical ones, using neurotransmitters, before converting
them to back electrical signals again. And you learned how cocaine is a sterling example
of how artificial imbalances in this electrochemical system can lead to dysfunctions of all kinds. This episode of Crash Course was brought to
you by Logan Sanders from Branson, MO, and Dr. Linnea Boyev, whose YouTube channel you can check out in the description below. Thank you to Logan and Dr. Boyev for supporting Crash Course
and free education. Thank you to everyone who’s watching, but especially to our Subbable
subscribers, like Logan and Dr. Boyev, who make Crash Course possible. To find out how you can
become a supporter, just go to This episode was written by Kathleen Yale,
the script was edited by Blake de Pastino, and our consultant, is Dr. Brandon Jackson.
It was directed by Nicholas Jenkins and Michael Aranda, and our graphics team is Thought Café.

100 Replies to “The Nervous System, Part 3 – Synapses!: Crash Course A&P #10”

  1. dear people in the comments:

    your reaction to learning that you are more complex than you thought shouldn't be 'ahh yes, I can explain all that I don't understand with God'. There's a range of life currently existing from the simplest (like algae) to the most complex (like us); you can even look at our own cells and trace steps of them becoming more efficient and complex (look up mitochondria, for example). Did God design it all? Maybe they did. Or maybe, like our ancestors who believed lightning to be from God, there are answers beyond your current knowledge that other people are pursuing. I'll stick with those who try to prove their ideas, rather than those who ask you to accept their ideas & not question them too much.

    I can learn about the details of evolution until I run into the limit of current knowledge. I can learn about 'God designed it all' for about 30 minutes until I run into 'sorry, you just have to have faith'. I'll be playing in the ocean of knowledge while y'all wade in the kiddie pool.

  2. The first time I got stuck in the shin by hockey stick when playing. This lead to a bundle of synapse nodules which grew. Each time I had a minor accident I had new bundle synapse nodules. Now thyroid because of cold water and curd. How to cure. Any possibility.

  3. It’s 7am, my test is at 10am

    I am literally crying, real tears. I’ve been studying this for weeks and been confused for weeks. You just took everything I thought I knew and made it all make sense

  4. Oh by the way i just wrote 9 papers full from your last 3 lectures. Im doing psych and focusing on bio psych. YOU ARE A HUGE HELP

  5. Is there a way to download the episode transcript? Like key terms, definitions, learning objectives etc.? Love the videos btw. U guys r AWESOME

  6. These videos are so awesome. Very helpful if you already know the material but are just brushing up after not studying for a while. Cracked up at the "take cocaine for example..don't take cocaine!" had tor rewind that a few times.

  7. For the young people that don't know the meaning of the crazy guy with a cocaine mustache holding two guns you need to watch Scarface so you will undesrtand 🙂 Thank you CrashCourse, amazing explanation.

  8. Ok so we know how a message is transmitted from one neuron to another.
    What I'd like to know is what happens to the synapses (or a large group of synapses) when one is trying to figure out 1+1=2?
    How does the synapse know if it should enhance, attenuate or block the signal? And what does it do when a symphony of the synapses act together to finally figure out 1+1 is indeed 2?

  9. Does anyone know how memory works? long term and short term memories? What role the synapses play in the process of storing and retrieving memories?

  10. Oh no I'm getting that same feeling when first introduced to trigonometry, an overwhelming sense of confusion. 😆😆😆

  11. "In popular culture and media, dopamine is often seen as the main chemical of pleasure, but the current opinion in pharmacology is that dopamine instead confers motivational salience;[3][4][5] in other words, dopamine signals the perceived motivational prominence (i.e., the desirability or aversiveness) of an outcome, which in turn propels the organism's behavior toward or away from achieving that outcome.[5][6]"

    (From Wikipedia.)

  12. Now I can think about how much is going on with my neurons when I'm trying not to fail my test.😃

  13. Now science is beautiful
    I wish all our lessons was like that

  14. When I graduate, I'm writing a thank you letter to Hank Green. Without him, I'd probably fail. 😂

  15. I wish people could make informative videos that don’t give me a headache like I’m listening to a late night infomercial. Too bad Billy Mays is dead, he’d be making a killing narrating science videos now. CALL NOW!!

  16. Bible says Jesus Christ is the Word of God and all of creation is pointing at God's system which is Christ

  17. I am in loooove with these videos! I wanna watch all of them and i also wanted to support but the link in the description wont work 🙁

  18. Takes teachers at my school 2-4 hours to teach this…..and we get bored…you did it in 10 mins and I loved every second…you guys help so many people through exams so please please don't stop doing what you're doing. Thank you so much x

  19. These videos are so helpful, I can’t believe I didn’t find this until the night before my test!

    My professor explained everything separately and never put it all together.

    Thank you so much.

  20. How does the neuron switch or choose? If neuron A fires off and it has 10,000 synapses to choose from, how does it know which ones to route to?

  21. @9:14 Hank says that preventing re-uptake of neurotransmitters can cause us to "lose receptors" as the body adapts. But wouldn't we actually gain receptors as a way of dealing with the increased amount of neurotransmitters hanging out in the synaptic cleft? Help resolve my confusion, folks!

  22. I prefer scientific thooo nowadays it's looking different, though I would appreciate the new videos but the old ones gets so many sci information in my brain that I like it

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