All right, good afternoon everyone. So continuing... on from where we got to last week then in human physiology and last week we were thinking about that kind of sensory information detection and that transmission into the central nervous system and we really focus mainly on the somatic nervous system and those somatic senses so today we're going to be continuing on but now we're looking at the motor output and so that kind of movement and Again, mainly thinking about the somatic nervous system, because we're thinking about skeletal muscle control, so those voluntary movements that we are actively choosing to do.
And we're also going to more specifically focus on the level of the spinal cord and motor control from the level of the spinal cord. So today then we're going to have a look at the different sort of fibers that make up our muscle and how they're innervated by different motor neurons and how these motor neurons are able to control smooth precise and the force of contraction of our muscle and then we're going to start thinking about bringing in those proprioceptors that I mentioned to you in the last lecture, those receptors that are associated and found within our skeletal muscle. So we're going to start thinking about those and how that sensory information is then relayed out as a motor output.
So for the first part, then, we're going to have a look at these muscles, and in particular, the alpha motor neurons that innervate the muscles and control contraction. So like I said, then, we're mainly focusing at the level of the spine. spinal cord. And in the spinal cord, we have these alpha motor neurons.
And these are the largest motor neurons that are found in the spinal cord. And they have their cell bodies here in the ventral horn of the spinal cord. So I'm sure I would have said to you last week that when we talk about the dorsal side, we're thinking sensory.
When we're talking about the ventral side, we're thinking motor. So these motor alpha motor neurons have their cell body here in the ventral horn and their axons extend out from the spinal cord towards the skeletal muscle. of the relevant parts of the body wherever that particular muscle is and they then innovate and sign up with the skeletal muscle and this is a a specialized type of synapse that's known as the neuromuscular junction and these these motor neurons on their synapse of the skeletal muscle is what is controlling um that contraction of the muscle these these motor neurons stimulate the contraction of the muscle for whatever movement is that we want do so our muscle then is a skeletal muscle is made up of a bundle of muscle fibers so you can kind of see in this image here we've got a particular skeletal muscle and it's made up of all these different muscle fibers that come together.
And we know then that we've got our alpha motor neurons extending out, our axons extend out, and synapse with these muscle fibers. Now, an individual alpha motor neuron, as you can see here. It's got a cell body here in the ventral horn of the spinal cord and its axon projects out but that axon can branch it's got all these kind of clatter as these branches and That means that a single alpha motor neuron is able to make multiple synapses with multiple different muscle fibers And we call this this kind of unit then the single alpha motor neuron and all the muscle fibers that is innovates We define this as the motor unit. Now what is important to recognize then, that each of these alpha motor neurons, they're able to make multiple synapses with different muscle fibers, but each muscle fiber only receives the input from the motor. from one alpha motor neuron.
So you can see in this diagram then, we've got these two alpha motor neurons, we've got a blue one and a purple one. You can see they're making multiple synapses of the different fibers, but each fiber only receives input from one of those, either the blue or the purple alpha motor neuron. And this is what we call focal innovation. This is quite important.
We don't want lots of inputs coming in necessarily into one. fiber because this will allow us to control that contraction a lot better. But it might kind of seem well this is a sort of one of those situations where you put in all your eggs into one basket. What if that alpha motor neuron doesn't fire properly, doesn't give enough signal to those muscle fibers, does that mean that you know we're not going to get proper contractions? we're kind of putting all our eggs into that one basket.
What if it doesn't work as well? We're not going to get that contraction. Now, there is a safety feature in place for this focal innovation to prevent this from happening, in that each of the alpha motor neurons they release a lot more of the signal that actually causes the muscle contraction than is actually required. That signal is known as acetylcholine, and they tend to release 8 to 10 times more than is actually necessary. So that means we've got a sufficient amount of that neurotransmitter present, so it's very likely to bind and cause contraction of our muscle.
So this is kind of that safety feature to this focal innovation. So I said then that these alpha motor neurons then, they synapse with the muscle fiber. And this is a specialized type of chemical synapse known as the neuromuscular junction. Now I know you've been doing a little bit with Vera about action potentials and what happens at the synapse. So hopefully you'll recognize that a lot of what is happening at this specialized synapse is very similar to a normal chemical synapse, but there are some unique features.
So what's going on then? So hopefully you all know then that the action potential comes down our axon, and in this case it's of our motor neuron, and it then reaches the axon terminal. And once it reaches the axon terminal, we're going to get a depolarization of our axon terminal, and that depolarization is going to trigger the opening of these voltage-gated calcium channels. And that opening of those channels is going to allow calcium to influx into the axon terminal. So we're going to move down that concentration gradient into the axon terminal.
And that's going to result in an increase in intracellular calcium within the terminal. And that calcium is really important because that rise in intracellular calcium is going to trigger... these synaptic vesicles that are containing the neurotransmitter, to move to and fuse with this presynaptic membrane, allowing that neurotransmitter to be released through a process known as exocytosis. Now, in our neuromuscular junction, then, the neurotransmitter that is present in these synaptic vesicles, found in the axon terminal of our motor neurons, is specifically acetylcholine.
So acetylcholine is the really important neurotransmitter. neurotransmitter at the neuromuscular junction that ultimately results in contraction of the muscle. So when the acetylcholine is then released into our synaptic cleft, so this small narrow gap between our axon terminal and our muscle fiber, it's then going to bind to receptors that are expressed on the muscle fiber membrane. And it's this very specific type of cholinergic receptor that is specifically expressed on these muscle fibers, and that is the nicotinic receptors. And these receptors are essentially ion channels.
So the binding of acetylcholine to these channels is going to cause the opening of these channels, and it's going to allow sodium to move into our muscle fiber and cause a depolarization in the membrane potential of our muscle fiber. And that depolarization, when it's in our muscle fiber, is what we call the end plate potential. So once acetylcholine is bind in its hand, its effect then, it then needs to be released from the synapse or removed from the synapse. And it's this important enzyme here, known as acetylcholine esterase, that breaks down the acetylcholine.
So it breaks down acetylcholine into choline and acetic acid or acetyl. Now, choline, that can be taken back up into our axon terminal, and it can essentially be kind of recycled back into. forming some new acetylcholine which we can package up in musicals and use again so a great recycling system the acetic acid then that's not taken back up and instead that kind of just diffuses out the synapse away from the area so it's not having any of its effect so this depolarization that we get down here then that ends plate potential eventually that results in an action potential and that is what is going to cause the contraction of our muscle allowing us to perform whatever movement it is that we want to do.
So acetylcholine from our motor neurons is controlling that contraction of our muscle. If you have a look at this diagram over here, this is an electron microscopy image. We can see a little bit more detail about this neuromuscular junction. So on this side of the image then, this is our nerve terminals. This is our axon terminal of our motor neuron, whereas this side of the image, this is all our muscle fiber.
And hopefully you can see then in our axon terminal, there are all these little circles everywhere. These are the synaptic vesicles that are containing the neurotransmitter, they're containing acetylcholine, and they tend to be clustered together in what we call active regions. Opposite then on the muscle fiber, hopefully you can see that the actual fiber, the membrane of our muscle, has this kind of folded structure to it. We call these the post-junctional folds, and it's actually here where those nicotinic... receptors are expressed so we tend to find that the sign the synaptic vesicles kind of cluster in the axon terminal in regions kind of opposite where the post junctional folds are that when they're released the acetylcholine can then directly bind to the nicotinic receptors present on the expressed and post junctional folds And just to kind of highlight then a particular toxin that actually targets the neuromuscular junction, known as tubocrarin.
And this is actually a toxin that's used by South American hunters. They apply it to the points on the end of their spears, and they use it in hunting. And the reason for this is because it acts to paralyze the prey, whatever they are that they're hunting. So it's going to paralyze the muscle.
And the way in which it does this is because it acts as a nicotinic receptor antagonist. So it can bind to these nicotinic receptors and essentially block and kind of prevent the action of acetylcholine. So that means acetylcholine can't bind and therefore can't cause contraction of the muscle. So instead we see this kind of paralysis of our muscle.
Hence why it's very good for hunting. So that's our neuromuscular junction then, and we can see that our alpha motor neurons are causing contraction of the muscle. But it's important that that contraction is smooth, and that's to prevent any jerky movements.
We want our movements to be smooth and controlled. This is achieved in a couple of ways. So firstly, each alpha motor neuron innervates muscle fibres that are spread throughout the muscle.
So it doesn't just innervate a collection of muscle fibres that are sort of clustered together. Each alpha motor neuron will innervate muscle fibres that are spread. throughout the muscle, allowing that muscle to kind of contract much more smoothly together as a whole rather than just individual sections. So you can kind of see that in this image here then, where we've got two different alpha motor neurons.
We've got our green one and and our yellow one. And hopefully you can see then that the muscle fibers that are in green, they're innervated by our green alpha motor neuron. And these are spread throughout that bundle.
And the same with the yellow ones. They're kind of spread throughout. They're not just clustered in individual regions. So that's one way that we ensure smooth muscle contraction. The second way is that the alpha motor neurons fire asynchronously.
So they don't just fire all together, they fire in this asynchronous pattern, again, allowing us to have this much more smooth, controlled contraction of the muscle fiber. So as well as smooth contraction then, we also want to make sure that our contractions are very precise. And this is particularly important for certain muscles that maybe we need a lot more fine control of.
And this sort of... precise contraction and how well we can be precise is related to the innovation ratio. And this relates to the number of individual muscle fibers that an individual alpha motor neuron.
innovates. So how many muscle fibers is it innovating? And this ratio is essentially inversely correlated with precision.
So if we have a look over here then we've got our alpha motor neuron and hopefully you can see its axon is branching and it's only innovating, it's only synapsing with a few muscle fibers. So that's a low innovation ratio and this is going to allow us to have very fine control. So if you imagine we have the rest of the muscle here A lot more muscle fibers.
A lot more alpha motor neurons, but they're only innervating a few of those muscles. It means we can kind of control each one individually, allowing us to have that much more fine, precise control for anything that's very dexterous, having to do small controlled moves. On the other hand then, if we have an alpha motor neuron that is able to innovate lots of muscle fibers, this is then a high innovation ratio and this is going to allow us to have course control.
So we're not going to be able to have our spine control. We can't have as much control over the individual muscle fibers. So if we stimulate this alpha motor neuron, we're just going to activate all these muscle fibers. We're not kind of reducing it down. And it kind of differs then, this innovation ratio, in the different skeletal muscle depending on what that skeletal muscle is for.
So for example then, that innovation ratio in our fingers tends to be very low. A bit like when we were looking at the sensory stuff last week, this makes a lot of sense because, again, we tend to explore our worlds with our hands and we're doing a lot of fine controlled movement. For example, picking up a pen or doing sewing. Whatever it is, we're doing these very small, very fine movements. In contrast then to our abdominal muscles, which are doing a lot less spine-controlled movement, and instead are doing those bigger movements, that bigger, coarser movement, for example, kind of holding up our posture, keeping the body in position.
So these have this much higher innervation ratio. We don't need to be quite so controlled and produce those spine movements. So, so far then, we've been talking about muscle being made up of muscle fibres, but there are actually two different types of muscle fibres that make up our muscle.
We've got the type 1, or also known as the slow twitch muscle fibres. And we've got the type 2, or also known as the fast twitch muscle fibers. Now, the type 1 muscle fibers, these sort of have a very slow contraction.
So when we activate them, they produce a very slow response, and they produce a low force of contraction. So it's not a really... heavy or high force, it's very low and controlled and slow force of contraction. And because they're only providing this kind of low, steady force of contraction, these are very resistant to fatigue. So they're able to maintain and sustain that contraction for quite a while.
One of the reasons why they can sustain that contraction is because we describe them as being oxidative. So what we mean by this is that these muscle fibers tend to generate their energy from the oxidative part of respiration. so they're going to be using glucose and glycogen putting that through glycolysis but also the oxidative part of respiration so oxidative phosphorylation and the electron transport chains they're going to be gaining lots of ATP from that respiration of those particular carbohydrates. So it means they're going to be getting lots of energy to maintain that contraction. And because they're oxidative, it means that they have a good blood supply.
They're going to need lots of glucose. They're going to need lots of oxygen. So they tend to appear this kind of red color. So that's about their kind of morphology then.
But thinking about their function, because they produce this very low sustained force contraction, they play a particularly important role in muscles that might be involved in, again, those very sustained contractions. For example, in maintaining posture and be present in our kind of abdominal muscles. So we need to maintain that contraction, but just a low, steady amount. Our second type then is these type 2, these fast twitch fibers. So these respond very, very quickly and produce a very high force of contraction.
So when we stimulate those and we release that acetylcholine, they're going to respond quickly, produce a high force of contraction. of contraction. That means that they're not able to sustain that contraction for very long, so they fatigue very, very quickly.
So we don't get sustained contraction with them. And one of the reasons is because these tend to be glycolytic. in nature. So they're using glucose and glycogen, but they're only putting that through glycolysis.
So we're only getting a small amount of ATP in order to sustain that contraction, which gets used up very quickly. And because they're not oxidative, it means that they don't tend to have as good supply, and they tend to appear more white in colour. But these are still important for certain functions, and in particular where we need very quick and rapid movements. So for example, in our eye muscles, we are constantly circading our eye muscles.
That's needing to happen very, very quickly, so they're quite dominant in those particular muscles. So it's important to recognize then that muscles, they are... made up of both types but one type might dominate more than the other depending on the particular muscle and the function of that muscle and it's also important to recognize then the alpha motor neurons they only innovate one type of that muscle that muscle. So we're not going to get an alpha motor neuron that can innovate both the slow twitch and the fast twitch. It's either going to innovate slow twitch or it's going to innovate fast twitch.
This is important because you can see that the function of these two muscles is very different. So we want to recruit them at different points depending on whatever the muscle and the contraction that we want to do is. So I mentioned then that we've got these two different muscle fibers and that they generate these different forces of contraction.
The slow twitch is that low force, the fast twitch is that very high force contraction. And generally then, we tend to recruit the... slow twitch fibers first but then as we pick up something heavier then we end up recruiting those fast twitch muscle fibers but again you know they they fatigue very very quickly due to their glycolytic nature So this is one way then that we can increase the force of contraction to recruit those fast twitch muscle fibers. But the other way that we could increase the force of contraction, if we wanted to pick up something heavier, is...
Firstly, to recruit more alpha motor neurons, so they're going to be stimulating more muscle fibres and causing more contraction. But the other way is to increase the action potential firing rate of our alpha motor neurons. So if we have a look over here then, we're looking at our action potentials of our alpha motor neurons, and we're recording the contraction of our muscle.
And we can see that in response to one action potential, so we get one load of acetylcholine being released, we get this contraction, this small contraction of our muscle. But if we were to increase the firing rates, we're getting constant release very quickly, one after the other, of acetylcholine. There isn't sufficient time for the muscle to relax, and so that contraction essentially summates. It gets bigger and bigger. with each of these action potentials that are coming along.
So we get that bigger force of contraction if we increase the firing frequency of our alpha motor neurons. There is, however, a kind of plateau point with this. We can't keep increasing the firing rate.
There is a sort of point where we can't increase it anymore, and this kind of maximum summation of our muscle fibres. And this is known as tetanus. And actually, the point where you get this kind of maximum summation essentially results in power. of the muscle fiber it can't contract anymore and it kind of stops contracting and that's what's known as testinus okay so summarize that first part then we've seen that our motor unit is made up of an alpha motor neuron and all the muscle fibers that it innovates and we know that an alpha motor neuron either innovates our slow twitch or our fast twitch muscle fibers they're in it in innovate one type, not both types. And it's dependent on the innovation and the recruitment of these alpha motor neurons that's able to control smooth, precise, and the force of contraction.
Okay, so moving on to the second part then. I'm going to introduce you to another type of motor neuron known as the gamma motor neurons and bring in what we learned in our last lecture about these prokaryote receptors known as the muscle spindles and Golgi tendon organs and their role in kind of mediating and controlling muscle contraction. So again, focusing on the ventral horn of our spinal cord, we know we've got these alpha motor neurons. So these are here in the sort of brighter green, and they have these axons that extend out the ventral horn and innervate our skeletal muscle, and they innervate the contractile.
part of the skeletal muscle controlling the contraction of our skeletal muscle through the release of acetylcholine at the neuromuscular junction. But they're not the only cells present in our ventral bone. We also have these very small cells known as Renshaw cells, so it's these ones here in orange, and we describe these as being inhibitory interneurons, and these synapse with these alpha motor neurons, and they're inhibitory because they release this particular type of neurotransmitter that inhibits, so it decreases the activity of the neuron it's synapsing with.
And that neurotransmitter is known as glycine. So this is the inhibitory neurotransmitter that we find in the spinal cord. And this, essentially, when it synapses with these alpha motor neurons, if it's releasing the glycine, it's then going to inhibit and reduce the activity of these alpha motor neurons. And it plays an important role in what's known as lateral inhibition. And this is essentially preventing over-contraction, over-activity of our muscle and enables fine control.
So if we have a little look over here, this is what I mean by lateral inhibition. So we know we've got our alpha motor neuron, cell body in the ventral horn of the spinal cord, and axon projects out towards the skeletal muscle. But this axon at the... level of the ventral horn of the spinal cord, so we're still in the spinal cord at this point, this axon branches, and one branch synapses with our Renshaw cell. So that means that that signal that's being passed...
along the axon to our skeletal muscle is the same signal that's being passed along this branch to the rencial cell. So that means the rencial cell is getting information about the stimulus, about the force of contraction. We've got that high frequency action potential coming along. We're going to get that high force of contraction and our rencial cell is going to pick that up. And if this signal is sufficient enough to activate our renshul cell, so in other words, we've got a big force of contraction about to happen, and it activates the renshul cell, that cell is then going to release glycine, which then...
binds to that same alpha motor neuron and essentially then inhibit, reduce the activity and therefore kind of reducing the signal, that action potential that's going out to our skeletal muscle. kind of without receiving the information that there's going to be a lot of work the wrench or so helps to reduce that and control it preventing damage from over contraction but this is also important for controlling fine and precise movements And it's these cells then that are actually the target of this tetanus bacteria. So this is where the term tetanus, that paralyzation of the muscle I mentioned a minute ago, gets its name from. So this bacteria talks.
sometimes you can get it kind of from rusty nails and things like that it essentially targets the glycine receptors and that are present on the motor neurons so it blocks them acts as an antagonist that means glycine can't act on it and therefore we can't reduce the activity of our alpha motor neurons so the alpha motor neurons keep sending out signals we keep getting contraction and that contraction summates so much we reach tetanus and we get the paralysis of the muscle fiber So the final type of cell then that's present in the ventral horn is another type of motor neuron known as the gamma motor neurons and these ones innervate the muscle spindle so they're not involved in controlling the contraction of the muscle as such like the alpha motor neurons. Alpha motor neurons control the contraction the gamma motor neurons instead innervate the muscle spindles. So looking at our muscle spindles in a little bit more detail then. So I introduced you to these in our last lecture, and I told you that they were called proprioceptors, but we can also describe them as mechanoreceptors.
So I told you that mechanoreceptors are the ones that are called proprioceptors. Interceptors are all about detecting this physical distortion. In the last lecture, we were thinking about them in the skin, so that was all to do with touch. But these are now present in our muscle. We're still getting physical distortion.
We're getting movement. of the muscle. So the two terms, proprioceptors and mechanoreceptors are kind of used interchangeably for these particular receptors.
And what they're detecting then is stretch in the muscle. So I've been telling you then that muscle is made up of these muscle fibers, but we can break down the muscle fibers a little bit more. So muscle fiber then is made up of this extrafusal muscle, so this is the part of the muscle on the outside. This is the contractile part.
This is the stuff that our alpha motor neurons are innervating and actually causing the contraction of the muscle. The inner part of our muscle fiber then, this is known as the intrafusal fiber. Now, the ends of this intrafusal fiber are attached to the extrafusal fiber, and they themselves are a little bit contractive. So they still move with the movement of the extrafusal muscle, but overall the intrafusal fiber is not described as being contractive.
They're the non-contractive part. And this center part, then, of the intrafusal muscle, this is the muscle spindle. So our gamma motor neurons then, they innervate kind of the ends of this intrafusal muscle to create that slight contraction of those end parts and control it there. And our muscle spindle right in the center then, that is going to be innervated by our sensory neurons but it's then going to be able to send in that information about muscle stretch into the spinal cord.
So, looking at our muscle spindles then, and those sensory fibers, those afferent fibers that innervate the muscle spindle. So, there are three types of intrafusal muscle, and they sort of differ mainly on their morphology and the kind of information that they are providing. So, the nuclear bag fibers, so these two types.
we've got the dynamic and the static they tend to have this kind of bulgy part to the center of them and the nuclei of all the muscle fibers tend to kind of be clustered together in this kind of bulgy center in comparison then to the nuclear chain fibers that have this much more slender slimmer morphology and the nuclei tend to line up in these rows in the center So what about the afferent fibers that innervate these intrafusal muscles then? Now, I introduced you to these last week as well, and I described them as being A fibers and C fibers. Now, unfortunately...
when we're talking about the afferent fibers that innervate muscles so our sensory fibers that innervating muscles we give them a slightly different name they're very similar but they've got a slightly different name this time they're group one two three and four but we're mainly focusing on group one and two okay but they respond very similar they look very similar in their morphology large diameter myelinated and so on So the two main types that are innovating our muscle spindle then are the group 1A. So this is essentially a subgroup of group 1. So there's a 1A and a 1B. It's the 1A that innovates the muscle spindle. and the group two that innovate the muscle spindle and the way that they innovate and the information that they send into the central nervous system varies slightly so the group 1a they innovate all three types of that muscle spindle and they have these kind of annular spiral sensory endings so this essentially wrap around these muscle fibers the intrafusal muscle or the muscle spindle and they are sending information about absolute stretch and change in stretch into the central nervous system group two then They only innovate the static nuclear bag fibers and the nuclear chain fibers, and they have these kind of what we call flower spray sensory endings. So they look a little bit more like a classic terminal, innovating these interfusal muscles.
And these only carry information about absolute stretch into the central nervous system. So a slight difference of what information that they are taking in. So a really nice example then of when our muscle fiber is able to detect stretch in the muscle and essentially result in what's known as a stretch reflex.
As a result of detecting the stretch by the muscle spindle, we then get a contraction of the muscle. This is a stretch reflex. And a really nice example is known as the knee jerk reflex.
So what's going on then? So this reflex essentially involves tapping the patella tendon that sits just below the kneecap now when you're doing this the patient has to be very relaxed they usually kind of sat on a table or a chair they need to be very relaxed and not usually looking at the person actually tapping the patella tendon because you can override the reflex So you tap the patella tendon, and this is going to cause a stretch in that muscle spindle. It's going to cause a stretch in the intrafusel muscle, which is going to activate that muscle spindle, that mechanoreceptor.
And that activation is then going to trigger that signal, those action potentials traveling along our 1A afferent neurons. So these are those sensory neurons that we've just looked at that have their cell bodies just outside the spinal cord, and those axons that project. from the muscle spindle all the way in to the dorsal horn of the spinal cord.
In the dorsal horn of the spinal cord, then, this is where that axon then branches. We get two branches. The first branch synapses with an alpha motor neuron in the ventral horn of the spinal cord.
and the axon of that alpha motor neuron projects out and synapses with the same muscle of where the muscle spindle was so it's going to synapse with the quadriceps and we're activating this alpha motor neuron with so we're going to get release of acetal choline our neuromuscular junctions and we're going to get contraction of the quadricep The other branch then, this doesn't directly synapse with an alpha motor neuron, and instead it synapses with one of those inhibitory interneurons, one of our Renshaw cells. And if we activate those inhibitory interneurons, That inhibitory interneuron is then going to release glycine. And that glycine then binds to an alpha motor neuron, which it's synapsing with, again, in the ventral horn of the spinal cord. This time, though, that alpha motor neuron, its axon, is sending projections to the antagonistic muscle. This is the hamstring.
So through the action of an inhibitory interneuron, then, we're then going to inhibit the action and the activity of this alpha motor neuron innervating our hamstring. So essentially, we're going to get contraction of our quadriceps, whilst at the same time we're getting this kind of reciprocal innervation of the hamstring. So we're kind of getting this antagonistic effect, and as a result, the leg raises.
Obviously, this all happens a lot quicker than the way that I would speak through it. But this is a really common reflex. flex path that's kind of tested in clinical setting to ensure that we are getting this appropriate innervation of skeletal muscle.
And this is a really nice way of kind of demonstrating the role of the muscle spindle in detecting stretch and the motor output that we get as a result of it. So the muscle spindle then is also important at kind of monitoring the muscle contraction and then correcting it when required. So the last one was the stretch reflex about triggering contraction of the muscle.
This one is all about kind of monitoring the contraction. contraction and correcting it when it's needed. So when we go to make a movement then we get this kind of information when we're actively deciding to produce a movement.
This information is going to come down from the brain from what we call these upper motor neurons. And these upper motor neurons synapse with both the alpha and the gamma motor neurons. And we get this kind of co-activation of both of these types of motor neurons. So because we're getting activation of our alpha motor neuron, we're going to get contraction of our extrafusal muscle, and the activation of our gamma motor neuron is going to essentially cause a slight contraction of the upper motor neuron. the intrafusal muscle and overall there is this kind of balance between contraction of the intrafusal and the extrafusal muscle so we don't get any stretch in our muscle spindle everything happens as expected however if we went to perform a particular movement I don't know picking up a box and then that box actually ended up being a lot heavier than we thought it was going to be that means there's going to be this imbalance between the contraction of our extrafusal muscle and the intrafusal muscle.
So we're not going to get enough contraction of our extrafusal muscle, and we're not going to be able to then pick up the box because it was heavier than we thought. But we will then get a stretch in our muscle spindle, okay, as we're attempting to pick it up. We're going to get this stretch in the muscle spindle.
That stretch and that imbalance between the two aspects of the muscle fiber is then going to activate that innovating sensory neuron that innovates our muscle spindles, so those type 1a afferent neurons. So that means we're going to get this action potential, again, traveling along the axons of our type 1 afferent neurons, all the way into the dorsal horn of the spinal cord. And these synapse directly with our alpha motor neurons, and it's going to activate those alpha motor neurons, encouraging them to release more acetylcholine at that neuromuscular junction.
so then increasing the contraction of our extrafusal muscle, which means then we'll be able to pick up that box that was heavier. We're kind of increasing the force of contraction. So there wasn't enough contraction, we weren't able to pick it up, that causes a stretch in the muscle fibre, which as a result sends that signal kind of relapsing. that signal back to our alpha motor neurons, getting them to work a bit harder, fire more action potentials, release more acetylcholine and contract the muscle further. And that entire reflex then is what we call the gamma loop.
So all about monitoring contraction and correcting it when required. So our second type of mechanoreceptor that I spoke about last week with them was our Golgi tendon organs. Again, associated with the skeletal muscle, but specifically they're found in the tendons.
that essentially allow our skeletal muscle to be attached to our bone. And again, these ones are all about kind of detecting of sensory information. So the muscle spindles is all about stretch, but the goal is to detect sensory information.
Golgi tendon organ is detecting muscle tension, this kind of force of contraction, how contracted the muscle is. And again, just like our muscle spindles, the Golgi tendon organs are innervated by sensory neurons. This time, it's the 1B sensory neurons, so that other half of our group 1 sensory neurons.
So the 1B sensory neurons, whereas it was the 1A and 2 sensory neurons for our muscle spindle. And the Golgi tendon organs then, they play an important role in another reflex known as the Golgi tendon reflex. And this essentially protects the muscle from overloading.
And this is kind of the inverse. of the stretch reflex. The stretch reflex is all about our muscle fibre detecting stretch and ultimately causing contraction. This time, the Golgi tendon organ is detecting a high force of contraction and resulting in a relaxation of the muscle. so reducing the contraction of the muscle.
So how does this work then? So we've got our Golgi tendon organ here in the tendon, and if we've got this very high force of contraction in our muscle, maybe too much that we're going to damage the muscle, that's going to increase the tension, and that's going to activate our Golgi tendon organs, which as a result is going to result in those action potentials, those signals, travelling along our 1B afferent neurons again into the dorsal. horn of the spinal cord.
This time then, our 1B afferent neurons, they synapse directly with these inhibitory interneurons. So again, activating an inhibitory neuron, and these inhibitory interneurons synapse with those alpha motor neurons. So if we activate the inhibitory neuron, we're going to reduce and inhibit the activity of the subsequent alpha motor neuron, so we get less action potentials firing. less contraction of the muscle, and essentially reducing that contraction, preventing it from overloading, preventing damage of our muscle. Okay, so to summarize our second part then.
So we've seen that there are two different types of motor neurons in our ventral horn. We've got the alpha motor neurons that innervate the extrafusal muscle, involved in essentially controlling the contraction of the muscle at our neuromuscular junction. with the release of acetylcholine. The second type, then, is our gamma motor neurons, and these ones innervate the muscle spindle to cause the contraction of that intrafusal muscle. And the muscle spindle is all about monitoring muscle stretch and are involved in the stretch reflex, so activating muscle contraction, but they're also involved in the gamma loops, the kind of monitoring and correcting the contraction.
Our other type of proprioceptor then was our Gowi tendon organ, this time monitoring muscle tension. And essentially, that reflex is all about the inverse of the stretch reflex, so relaxing the muscle, preventing over-contraction. Okay, so ending with the quiz as usual.
Which statement is false regarding alpha motor neurons? So A, they innervate extra fusel muscles. A single alpha motor neuron can innervate slow and fast twitch. muscles.
Alpha motor neuron innervation of muscle fiber is spread, not clustered. And the fewer the muscle fibers a single alpha motor neuron innervates, the higher the precision of muscle contraction. So which one is false?
Which one's incorrect? Hands up for A, B, C. And D, that all felt very confident for almost 6 o'clock on a Tuesday. Yes, the answer is B.
So they either innovate slow or fast twitch, depending. How can increased force of muscle contraction be achieved? Do we reduce the action potential firing of alpha motor neurons?
Do we increase the action potential of gamma motor neurons? Do we recruit type 1 or recruit type 2 muscle fibers? Hands up for A, B, C, and D. Yeah, perfect. So don't be fooled by this one with B.
If we increase the firing of our alpha motor neurons, then that would increase force of contraction. Okay, question three. What two main types of afferent fibers innervate muscle spindle?
Is it 1A and 1B, 1A and 2, 1B and 2, or 2 and 4? Hands up for A, B, C, and D. Yeah, perfect.
So 1A and 2. 1B innervates the golgi tendon organ. Question four. If you went to pick up something that was heavier than you thought it was going to be, what reflex would be initiative?
Is it the myotactic reflex, the withdrawal reflex, the gamma loop, or the Golgi tendon organ reflex? Hands up for A. B, C, and D.
Yeah, exactly. Gamma loop. All about that co-activation.
Thank you very much, guys. I think Vera said that the summary lecture tomorrow has been cancelled. There was no questions submitted.
But there's opportunities later in the module.