Health and medicine
Learn about the role of voltage gated calcium channels in triggering synaptic vesicles to release neurotransmitters. See how the frequency and duration of action potentials influence the amount and duration of neurotransmitter presence in the synaptic cleft. Created by Matthew Barry Jensen.
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- What is a voltage calcium channel? I'm confused.(2 votes)
- Voltage-gated calcium ion channels are just another type of ion channel found in neurons. The shape of the calcium channel protein allows only calcium ions to pass through the channel.
Changes in voltage due to the action potential cause the voltage-gated calcium ion channels to open, allowing calcium ions to move into the cell. There the calcium ions interact with the neurotransmitter containing vesicles (membrane-bound containers) causing them to fuse with the cell membrane, and release the neurotransmitters into the synaptic cleft.
Other ions like sodium or potassium do not interact with the vesicles, which is why the voltage-gated calcium ion channels are necessary.(16 votes)
- why only ca, na, & k ions and where do they come from. Why do only these specific ions interact with the neurons?(2 votes)
- I understand there are divisions of the nervous system, ie the autonomic system is divided into two systems the sympathetic and the parasympathetic , now I find this vague in a way, nerves are real like wires or thin tubes do the parasympathetic and sympathetic use the same nerves like cable companies or does each system have its own hardware ie its own set of nerves.
- They have their own neurons (their own hardware if you will) assuming you are talking about the effector neurons for each system.(3 votes)
- That video was great, thanks, and I'm now fully good with how the neurotransmitters are released. What I'm still not understanding is how the vessicles manufacture the neurotransmitters inside the pre-synaptic cleft. Once they have released, how do they 'fill up' again? Thanks!(3 votes)
- Take a look at the next video, "Neurotransmitter removal". It shows how the combination of reuptake by the presynaptic membrane, and astrocytes recycling neurotransmitters can "fill up" vessicles again:
- the release of the ca is not depend on the strength of the action potential?
because they equal?(1 vote)
- The release of calcium is dependent on the frequency of action potentials. Action potentials have a defined waveform and time course. The frequency of the action potentials is in turn dependent upon the intensity and duration of the stimulus.(5 votes)
- I'm sure it varies by nerve terminal location, but about how long does it take for calcium to diffuse across the synpatic cleft?(3 votes)
- I don't know the time but it is extremely small, possibly on the micro second scale. Think of this: when your mind tell you to lift your arms then you can do this almost immediately even though the signal from your brain to your arms goes through many nerves and nerve endings.(1 vote)
- In general Is the chemical medium of the neuro transmitters signal thru put faster than the shortest time between action potiental spikes? For example, if the time between ap spikes were 10 ms would the neuro transmitters babe able to complete a complete cycle before the next ap spike?(2 votes)
- Yes. Usually each spike invading the axon terminal will produce a distinct response in the post synaptic neuron.
Interesting things can happen at inter-spike intervals that brief. For example, short inter spike intervals can change how much neurotransmitter is released per spike. If two action potentials invade an axon terminal 10 msec apart, this can actually result in more transmitter being released on the second pulse than on the first pulse. This is called "short-term facilitation."
On the flip side, axon terminals can deplete their stores of neurotransmitter if exposed to persistent, high-frequency activity. In this case, the response in the post synaptic neuron weakens or "depresses" and can even disappear.
Short-term facilitation and depression are two examples of how the history of activity at an axon terminal can affect how it responds to subsequent spikes.(2 votes)
- At4:16, he states that neurotransmitters will stop being released once the action potential stops. What happens if there are neurotransmitters still left in the synaptic cleft that are not attached to postsynaptic membrane receptors?(2 votes)
- I'm not sure i understand why the v-gated Ca++ channels open. The AP causes the interior to become more positive. So wouldn't this mean the Ca++ ions would be repelled from coming in? Or is the concentration gradient able to overcome this?(1 vote)
- Remember that the gradient is actually the "electrochemical gradient", meaning it has an electro (the + and - charges) and chemical (the concentration gradient) aspects. This is just good to keep in mind throughout the lecture.
As for calcium, you may need to think of it a bit differently. The electrical signal that runs through the neuron causes depolarization and repolarization over and over, this is so that the electrical signal be propagated. But after it "moved on" to the next gate, the previous one closed. So the previous one is no longer positive.
Once the signal reaches the end of the neuron, it needs to go to the next neuron. But it can only do so by storing itself into molecules. There is electrical difference between the neuron A and B. So the electrical signal triggers the opening of Calcium channels. Calcium rushes in because of the concentration gradient, and it stimulates the release of vesicles. These vesicles already have neurotransmitters, and they release them outside of the neuron.
So, in effect, the energy is being transferred from electric to chemical (remember electrochemical?) energy. Once the neutrotransmitter binds to the next neuron, it causes the Na/K action potential to start again and this cycle repeats.
I hope this was a bit clear!(3 votes)
- So what's an example of a NT that is released upon Ca influx? And when such a NT diffuses across synaptic cleft and binds to Ligand Gated channels on the post synaptic membrane, what in an example of what could happen?(2 votes)
Voiceover: In this video, I want to talk about how neurotransmitter is released at the synapse. In the last video, we went over the structure of a typical chemical synapse with an axon terminal like I've drawn here in green that have synaptic vesicles full of neurotransmitter and we talked about how on the postsynaptic membrane of the target cell, there are receptors for those neurotransmitter molecules, but the question is, how do the neurotransmitter molecules get out of these synaptic vesicles in the axon terminal to cross the synaptic cleft and bind to their receptors? To understand neurotransmitter release, we need to talk about this new type of ion channel. This is a voltage gated calcium channel. We talked about voltage gated sodium and potassium channels when we talked about the action potential that at the axon terminal there are these voltage gated calcium channels that play a big role in neurotransmitter release. When the action potential comes down the axon and reaches the axon terminal, the action potential will change the membrane potential at the axon terminal and it will open these voltage gated calcium channels. When these voltage gated calcium channels open, calcium will flow in to the axon terminal because that's at a much higher concentration outside the neuron than inside the neuron, so it will flow in and increase the concentration of calcium here inside the axon terminal. And you just draw a couple of these, but there are lots of them, of course. The increase concentration of calcium inside the axon terminal when these voltage gated calcium channels are open are going to cause changes to proteins on the synaptic vesicles and proteins on the presynaptic membrane of the axon terminal and they're going to cause them to interact and fuse, so let me just erase these little bits of membranes here and draw how these are actually fusing together so that now the inside of the synaptic vesicle is actually in communication with the outside of the neuron with the synaptic cleft. And then by diffusion, the neurotransmitter molecules will exit the axon terminal and they'll flow out into the synaptic cleft and there will be lots of neurotransmitter now in the synaptic cleft where there wasn't before. And remember, I've drawn this too large, it's actually a very small distance, so the neurotransmitters has no problem diffusing across and binding to its receptor on the postsynaptic membrane of the target cell. Now, recall we talked about the information contained in action potentials is really contained in the frequency and the duration of a train or a series of action potentials being fired down the axon of the neuron. Well, that information is now going to be converted into the amount and duration that neurotransmitter is present in the synaptic cleft and the way that that happens is that an increase frequency of action potentials reaching the axon terminal will cause more openings of these voltage gated calcium channels, so they usually more calcium will flow into the axon terminal and an increase concentration in the axon terminal will cause more synaptic vesicles to fuse with the presynaptic membrane so that a greater amount of neurotransmitter is released into the synaptic cleft and the longer duration of a train of action potentials will cause neurotransmitter release to occur over a longer period of time, so there's a longer duration of neurotransmitter being present in the synaptic cleft. So this is the way the information contained in the frequency and duration of a train of action potentials is converted into the amount and duration of neurotransmitter present in the synaptic cleft and that information is passed on to the target cell by a neurotransmitter binding to the receptors and the number of receptors that binds to and the duration of time the neurotransmitter is bound to receptors is related to the amount and the duration of neurotransmitter in the synaptic cleft. And when the train of action potentials stops firing the voltage gated calcium channels will close, calcium will stop flowing into the axon terminal and the normal processes that push calcium out of the neuron will quickly lower that concentration of calcium in the axon terminal and synaptic vesicles will stop fusing with the presynaptic membrane and neurotransmitter will stop being released.