Term
| When an action potential reaches the end of an axon, it |
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Definition
| causes the release of a neurotransmitter, or transmitter, into the synapse—a small cleft between two neurons or a neuron and muscle cell |
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Term
| Information, in the form of neurotransmitters, moves across the synapse FROM |
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Definition
| the axon on the presynaptic cell, TO the target cell, or the postsynaptic cell |
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Term
| Postsynaptic potentials are |
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Definition
brief changes in the membrane potential of the postsynaptic cell in response
to a neurotransmitter |
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Term
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Definition
| is an increase in membrane potential—the interior of the membrane becomes even more negative and farther from zero |
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Term
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Definition
| is a decrease in membrane potential—the interior of the cell becomes less negative and closer to zero |
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Term
| Excitatory post synaptic potential (EPSP) |
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Definition
| produces a small local depolarization as Na+ channels open, pushing the cell closer to threshold (ligand-gated channels opened by neurotransmitter) |
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Term
| Inhibitory postsynaptic potential (IPSP) |
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Definition
| produces a small hyperpolarization, pushing the cell further away from threshold |
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Definition
| chlorideions(Cl–)entering the cell, making the inside more negative (GABA activates Cl channels- GABA receptors) |
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Definition
Now we can see here an example of IPSPs and EPSPs in an experimental set up. So let's unpack this a little bit. We have three neurons here. The yellow neuron is the postsynaptic neuron, postsynaptic neuron. It's receiving inputs from two other cells, the red cell, which is a presynaptic neuron. It's presynaptic neuron 1. And the blue cell which is presynaptic neuron 2.
If we stimulate cell 1 to fire an action potential-- so what we're going to do is we're just going to inject a bunch of sodium into this cell directly through this electrode. And we're going to say, make an action potential. And we're going to record what happens in this cell when we do that. So when we do that, here is the red cell making an action potential. That's no surprise. But what happens in the postsynaptic cell is we see a little depolarization, an EPSP, an Excitatory Postsynaptic Potential.
If we stimulate the blue cell to fire an action potential, and we record right near where it's releasing its neurotransmitter, right near the synapse that it has with the postsynaptic cell, we see here is the blue cell's action potential. But what happens on the postsynaptic cell is we have a hyperpolarization of its membrane, or an IPSP.
Now, for this neuron, the postsynaptic cell to fire an action potential on its own, it needs to have some kind of excitatory driving input. Well, let's say that presynaptic neuron 1 got lots and lots of activation and started firing action potentials one after another. And each time it did, it took this EPSP and raised it up a little higher and a little higher. It might eventually make this cell go to threshold and fire its own action potential.
But if at the same time we stimulated this cell to keep on firing action potential after action potential, the IPSP that results would get larger and larger and that would interfere with the ability of this cell to generate enough excitatory postsynaptic potentials to make an action potential.
This is called summation. A combination of inputs to a single cell are summed over time and space. And if there's sufficient excitatory potential, the cell may generate an action potential. But if there is sufficient inhibition of the excitatory inputs, that can inhibit the cell from generating an action potential. |
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Term
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Definition
| . A combination of inputs to a single cell are summed over time and space. And if there's sufficient excitatory potential, the cell may generate an action potential. But if there is sufficient inhibition of the excitatory inputs, that can inhibit the cell from generating an action potential. |
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Definition
So let's look a little more closely at what happens at the synapse when an action potential has traveled down from the cell body down through the axon into the nerve terminal. This is an example of neuromuscular junction or a neuromuscular synapse. But all synapses operate on similar principles.
So here's a motor neuron. This is an alpha motor neuron from the spinal cord which you may have seen in a gross anatomy lab. And these have long axons that travel out into the periphery and form synapses with skeletal muscle. And when these neurons fire action potentials, they make skeletal muscles contract.
So how do they do that? So here's the action potential travelling down. Now, let's remember what's happening with an action potential, right? The membrane here is depolarizing a lot. In fact, it's becoming positive temporarily. And that depolarizing wave is spreading throughout the axon and then to the axon terminal, or the nerve terminal.
Now, the depolarization, once it reaches the nerve terminal does something really neat and something that should seem kind of familiar, it activates a voltage-gated calcium channel, a calcium channel. And that's important because calcium causes vesicles in the terminal to fuse with the membrane and secrete their contents. So calcium causes secretion. And the vesicles in the nerve terminal contain acetylcholine, the neuraltransmitter of the neuromuscular junction.
So the acetylcholine, the vesicles fuse with the membrane and acetylcholine is released into this synaptic junction or this neuromuscular synapse. And it binds to acetylcholine receptors on the muscle cell itself.
These acetylcholine receptors are ion channels that when they're bound to acetylcholine allow sodium into the cell and cause local depolarization that can lead to muscle contraction.
So why don't muscles stay permanently contracted? And the reason for that is because the neuromuscular junction also contains enzymes that break down acetylcholine. And this is true at all synapses. There's some mechanism to get rid of the neurotransmitter. Because neurotransmitters should not stay permanently in synapses.
The beauty of the nervous system is that we can have small, short-term local communication that can be very specific and that doesn't last permanently. If you keep a synapse running, you're going to wind up with tetany, a muscle that won't come out of contraction. Then you can't do anything. Or in the brain, you might wind up with a seizure where you have neurons just firing like mad and out of control.
So you have to release neurotransmitters and then move them on. In the neuromuscular junction, they are removed by breaking them down by acetylcholinesterase, acetylcholinesterase which makes acetate and choline. The acetate is lost to the circulation and then it's removed. And the choline is taken back up and used by the neuron to make new acetylcholine. |
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Term
| What Gates the Channels That Make EPSPs? |
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Definition
• Ligand-gated ion channels
• Neurotransmitters can
bind to receptors on the postsynaptic neuron and
activate ion channels.
• In this case, Acetylcholine activates a sodium channel
that causes an EPSP on a muscle cell.
• These are not the same as the voltage-gated channels |
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Term
| Why doesn’t the muscle just stay depolarized? |
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Definition
Neurotransmitters are either inactivated or taken back up (reuptake) by presynaptic terminal.
• Cholinesterase inhibitors: Sarin, some pesticides, Neostigmine
• Curare-frog poison: Blocks Ach binding to its receptor in muscle
• Botulinum toxin: prevents Ach
release from the presynaptic terminals
• Latrotoxin: causes all Ach to be rapidly released
• Hemicholinium: blocks choline reuptake
Some neurotransmitters, like serotonin, are taken back up and re-used. Selective serotonin re-uptake inhibitors (SSRIs) prolong the action of serotonin in selected synapses |
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