Week 2 Motor Control & Basal Nucleus Flashcards
When we are looking at the initiation of movement, the end product that we do require is the contraction of musculoskeletal fibers. And when we are considering for that, the first thing that we need to consider is the action potential signal that is reaching down to the motor end plate and releasing acetylcholine and resulting in excitation of the neuromuscular juncture. And so hopefully this is just an overall review of action potentials and tetany, or at least this slide here. And what we’re looking at is on the horizontal axis, we are looking at the frequency of action potentials, the frequency of the (EPSP/IPSP) that is getting down to the neuromuscular junction. On the vertical axis, we are looking at the overall force that’s produced.
A)
So if we take a look at the picture in A, in the blue box, what we see is repeating stimuli, but it’s at a fairly low frequency. So now is this temporal summation or is this spatial summation? As we’re looking at this, what we do see is as there is an action potential, we see a rise in force production. And then as the action potential disappears, we see a steady reduction in force back to baseline levels. Once it reaches baseline levels again, if we provide a twitch stimulus and we see a small bump in force, but again, a slow reversal and decay. We don’t see a great amount of force production at the muscle unit. What we’re looking at is it’s a (low-/high) frequency and it’s not enough to produce any type of meaningful force.
B)
Here as we increase the hertz to 37.5 hertz or higher frequency of EPSPs coming down. What do you see? You start to see (less/more) force production happening. So in this picture, what happened? We see a force production and then we see a decay. Here there’s a force production. But before there is enough decay to go back to baseline, you produce another action potential. Well, that pumps it up a little bit more, starts to go back down to the decay level. But again, before it goes back down to the baseline decay level, you add another twitch, EPSP, and you have another bump in force. You continue to do that. You see a rise in force. But if we take a look at the curve, at the force production, it’s not smooth. But we are starting to get a summation of force production due to summation of the EPSPs that are coming down to the neuromuscular junction.
C)
We speed up that frequency to 50 hertz. And what do you see as we start to get closer approximation of these EPSPs, we start to see (lesser/greater) force increase. So there’s a summative impact of force on the overall frequency of action potentials that are coming down to the neuromuscular junction from the primary (motor/sensory) cortex via our (ascending/descending) tracks. But it’s still not smooth. It’s not going to be smooth until we reach this fused tetanus where the contraction, where the action potentials are happening relatively quick.
D)
So now we’re looking at 120 hertz and we get a significantly (lesser/greater) force production. And it’s a smooth motion. So what we want to appreciate about muscle contraction is the frequency of EPSPs. The summation there matters.
EPSP; low; more; greater; motor; descending; greater;
The Henneman size principle is a very important muscle physiology and movement coordination principle. And really what we are looking at in the Henneman size principle is that the size of the motor unit and the overall EPSPs matter. So for dealing with a smaller motor unit versus a larger motor unit, a smaller motor unit is going to require (lower/higher) frequency of EPSPs to be able to produce a contraction. There’s (less/more) surface area. So there’s overall (less/more) EPSPs required to get to AP summation. So surface area and EPSPs are directly proportional.
lower; less; less
Let’s just focus on action potentials in muscle contraction at this point in the game. If we are looking at that perspective, what are the first types of muscles that are being called into play? First thing you gotta do is you have to stabilize the joint. And then you can get the joint through movement. Basic principles of human movement. I do believe that shaker introduced the idea of Punjabis neutral zone hypothesis in kinesiology - You need to be able to stabilize the joint first. You need the local muscles around the joint to stabilize. Ex: The rotator cuff musculature (before/after) the deltoids kick in before you can get excursion of the joint. And if we consider the overall size of the rotator cuff to the deltoid, which have greater size? The rotator cuff muscles, at least individually are smaller than the overall deltoids which are driving the motion. And the way we get that is a neural recruitment that relies on the frequency of EPSPs. So when we first initiate a movement, the first thing that’s going to happen is we’re going to start sending EPSPs, but they’re going to be (low/high) in frequency. As we continue to move the frequency (decreases/increases). The impact of that is as we start movement, the lower frequency of action potentials is going to stimulate activation of the (smaller/larger) muscles, the stabilizing muscles. As movement increases, frequency increases, and the (smaller/larger) muscles are called into play. So the way that the central nervous system prioritizes muscle recruitment is based on the frequency of action potentials that are reaching the muscles.
before; low; increases; smaller; larger;
There’s also this idea of low demand versus larger demand. So as we have low demand, you don’t need a whole lot of muscle. I should say there’s a low frequency of EPSPs that are getting down to the motor end unit that results in a smaller muscles activating. Now we’re talking within muscle groups. As you start to require greater demand, firing frequency (decreases/increases) and you have (smaller/larger) muscles being called into play. So let’s break that down into the elbow just because it’s a little bit easier to comprehend. With lower demand, it is a (lower/higher) frequency action potential. What are the smaller muscles in the elbow that result in elbow flexion? That’s going to be the brachioradialis probably, it’s not going to be the brachialis. The brachialis provides the overall size and strength of elbow flexion while the brachioradialis is smaller and helps to initiate the motion from a kinesiologic perspective. So in low demand, there is (lower/higher) amount of action potentials that are happening. As the demand increases the central nervous system (decreases/increases) the frequency of the EPSPs. And that shift in frequency is going to result in recruitment of the (smaller/larger) muscles.
increases; larger; lower; lower; increases; larger
I just want to review what a motor unit is. As well as the difference between that and motor neuron representation, as well as cortical representation. Precision of language counts when we are talking the science of medicine. So what is the motor unit? The motor unit is the motor neuron and the muscle fascicles within a muscle that the motor neuron is innervated. You might have several motor units within a particular muscle. So what are we talking about when we’re talking about a smaller motor unit versus a larger motor unit? A smaller motor unit might have a motor neuron and 10 fascicles and a larger motor unit might have one motor neuron and 50 muscle fascicles. Now, if you take one muscle, muscle A that has 100 fascicles, and muscle B that has 100 fascicles. Muscle A has 100 fascicles and 10 motor units innervating that particular muscle. So each motor unit has 10 fascicles within it. Muscle B, again has 100 fascicles, but it has 50 motor units in it. So now each motor unit is responsible for two fascicles, which is the larger motor unit, which is going to have more fine motor coordination? The one with 10 motor neurons innervating the muscle, or the one with 50 motor neurons? The more motor neurons you have going into a particular muscle, the (less/more) fine motor control you’re going to have. So consider the hand versus the elbow. What does that reflect? That’s also going to reflect cortical representation within the homunculus. If we go back to the prior semester, the more fine coordination that the muscle requires, the (smaller/larger) cortical representation it’s going to have. So while there’s a relationship between motor neuron representation and cortical representation. Motor unit size is based on the motor neuron and how many muscle fascicles, how many bundles of muscle fibers that motor unit is responsible for.
more; larger;
The action potential shift that we talk about is something that we call rate coding. Rate coding is the shift in action potential frequency relative to demand, so it has a specific name to it. From a muscle activation frequency perspective, slow twitch muscles are recruited with (lower/higher) action potential frequencies, whereas fast-twitch muscles are recruited at (lower/higher) frequencies. So slow twitch muscles (lower frequency), they need to be on, they need to be on for a (shorter/longer) amount of time to be able to provide stability for the joint. Whereas fast-twitch muscles are there to pick up the slack when the demand needs it. From a central nervous system perspective, how do we signal down to the end organ that we need someone to pick up the slack? You (decrease/increase) the frequency of the action potential. So while this might sound like just semantics and minutiae, as we consider these differences across tonic versus phasic muscles, we want to consider intervention intensity and intervention prescription. So there is direct relationship in terms of this muscle physiology (Henneman size principle), as well as rate coding and the frequency. Because from an intervention perspective, as you are trying to get overload of the musculature, how do you provide the right overload? If we are dealing with a slow twitch muscle or a smaller motor unit, how do we provide the adequate overload from an intensity perspective to be able to target activation of that particular muscle? If we’re targeting a phasic muscle or if we’re targeting a muscle that has a greater amount of fast-twitch fibers, how do you manipulate your intervention intensity and the prescription of your interventions to be able to target that phasic muscle? So those are things that I just want you guys to keep in mind as you go through your examination and intervention topics as you start to consider the principles of exercise physiology, and you start to apply the scientific principles to exercise prescriptions.
lower; shorter; increase
First, the movement has to be initiated. First. The movement has to be allowed by the central nervous system. And how does that occur? It’s not simply just the individual deciding, Hey, I want to move and there’s an execution signal that is being sent down to the descending signals. There is a lot of control that occurs to keep the movement system at rest. And then to get that system to get out of rest and result in a contraction. And what we’re looking at there from a neural organ perspective is the (cerebellum/basal ganglia).
basal ganglia
INFO ONTHE PICTURE IS SUFFICIENT
As you start to go into your content on Parkinson’s disease in neuro examination and intervention to what you see is individuals with Parkinson’s disease have a resting tremor sometimes. They have an overall unsteadiness, shakiness to the individual, and that shakiness would be present while they were walking. But if they increased the amplitude of their motion to a running pace, movement would become smooth. So there was something about this condition that was different based on the information that they had at the time and the clinical exams that they were able to perform. James Parkinson knew that the problem probably was not due to a corticospinal tract, but it was something with respect to the movement system. He termed the disorder extra pyramidal. Extra pyramidal is a word that continue to be per separated for a very long time with respects to conditions that involved the basal ganglia. It is not a term that is considered appropriate today. It’s not a term that we typically use, but you still need to be aware of it because there are some people that still use this term. As we would go on and continue to investigate and learn more about the condition. We started to learn about a structure that we began calling the basal ganglia and Parkinson’s disease as we know it. And the clinical features were tied to the basal ganglia. As we continue to study the structures we started and better sense of what the basal ganglia was responsible for.
Got it
Globus Pallidus - (cerebrum/brainstem) ?
Caudate - (cerebrum/brainstem) ?
Putamen - (cerebrum/brainstem) ?
Nucleus Accumbuns (reward, reinforcement, learning) - (cerebrum/brainstem) ?
Substantia Nigra/ ventral tegmental area??? - (cerebrum/brainstem) ?
Subthalamic nucleus - (cerebrum/brainstem) ?
The term basal ganglia is switching over to basal nuclei because ganglia are a collection of neuronal cells that we find in the (central/peripheral) nervous system. In the central nervous system, a collection of neurons with similar function are referred to as (ganglia/nuclei). So again, we have a shift in terminology, but it hasn’t picked up pace yet. There are a lot of functions associated with the basal ganglia and the one that we are going to focus on today is initiation of movement and inhibition of unwanted movement. But the basal ganglia also has a large role in learning, both motor learning and behavior learning, as well as reinforcement of behavior through reward versus punishment system (stimulus and response if you go back to psychology terms). So the basal ganglia has quite a few different functions that appear unrelated. But as we start to go through learning and reinforcement, they might be more interconnected than we think.
peripheral; nuclei; cerebrum; cerebrum; cerebrum; cerebrum; brainstem; brainstem
So first we’re going to start with a structure that we refer to as the striatum. The striatum is the _____ and ____. So here (referring to pic to the left), we’re looking at the brainstem right through here, medulla pons, start of the midbrain and then sitting within the cortical region. So we’ve got the lateral ventricles. And this, we looked at this picture before when we were discussing the corona radiata and the internal capsule. And if we take the corona radiata and the internal capsule away, it exposes the view of the caudate and putamen sitting here. Caudate - Now you’ve heard the term cauda equina and caudal meaning towards the tail. Cauda equina - horse’s tail. Caudate here refers to that which has a tail. So from the caudate coming through we’ve got the tail end. And then this structure sitting below, is referred to as the putamen. Collectively, these two structures are referred to as the striatum.
My sneaking suspicion is that that terminology is going to start going away soon because we’re starting to discover at some point, we thought that the connections to the caudate and putamen were (different/similar) and that they had similar functions because of how close and connected they are physically. What we’re starting to see is that the connections and the outputs might actually be very (similar/different).
caudate and putamen; similar; different
Just like we had a naming convention for ascending and descending pathways. Basal ganglia/basal nuclear structure’s have a naming convention. So if it has anything to do with the striatum/caudate and putamen, it’s going to start or end with “____”. So if we just make something up striato-cortical, it’s going from the ____ to the _____. Cortico-striate - It’s going from the _____ to the _____. I do want you to be aware that pathways that have the word striato in them are either coming from or going to the _____ and ______ .
striato; striatum; cortex; cortex; striatum; caudate and putamen
When we take a look at the anatomical relationship of the caudate and putamen with respect to the other surrounding structures. Let’s just first start with the shape of the caudate. The anterior aspect is big and bulbous and then starts to get thin as it starts to tail off towards the back (the tail portion). This large bulbous area, is very close to the frontal/prefrontal cortices. So think of the functions that the frontal lobe is responsible for (motor control, cognition, personality). So the thought was that because the front of the caudate is so big that it might be more associated with (frontal/occipital) lobe function and the cognition and judgments that are coming from that perspective. So it might have a (larger/smaller) role in cognition. And then as we tail off here, right at the end of the caudate is the amygdala, which is the center of fear. Sitting just adjacent to the amygdala at the tail end is a structure that we call the hippocampus, which is responsible for memory and navigation. So the memory aspect attaching on to the caudate reinforced the idea that because the amygdala and the hippocampus are so close and attached to the caudate, maybe the caudate is more responsible for learning and behavior. And then when we take a look at the putamen here, sitting just behind the putamen is the (cerebellum/thalamus). Think of all the sensory and motor pathways that are going through the thalamus, whether it’s to get to the brain or coming from the brain. They’re going through and connecting with the thalamus at some point. And with the thalamus being right next to the putamen, the thought was, hey, maybe the putamen is more associated with (vision/movement). And that certainly came to pass as we started to look at investigations though neuronal activities with fMRIs to determine, hey, what actually happens? And so we start to see that there is a specificity of connection and location. Within the caudate and putamen are the striatum. So in this particular picture (pic to the right), out of your textbook, when an individual is asked to perform some sort of a movement and we collect FMRI while the person is doing that task from the striatum (A is lateral, B is the medial aspect), we see a lot of activity happening within the (caudate/putamen), whereas we don’t see a whole lot of activity coming from the (caudate/putamen). This study and some other studies that have come after seemed to suggest that the caudate and putamen have fairly disparate functions. So how we might be getting away from referring to these structures as the striatum and referring to them individually as the caudate and putamen with respects to their individual function.
frontal; larger; thalamus; movement; putamen; caudate;
Next structure on the docket is the globus pallidus. If we take the caudate and putamen away, we have the thalamus sitting here (above the red arrow). And then inferior lateral to the thalamus is this structure here that we referred to as the globus pallidus. And just globally, the globus pallidus is responsible for controlling (conscious/unconscious) motion. The globus pallidus separates into two parts, globus pallidus (anternus/internus) and globus pallidus (posterunus/externus). They have different functions with respect to output. From a general perspective, the globus pallidus internus is there to (exhibit/inhibit) movement. Where as the globus pallidus externus is there to inhibit other portions of the (cerebellum/basal ganglia).
conscious; internus; externus; inhibit; basal ganglia;
From a pathway perspective, pathways that contain the globus pallidus have the word “_____” in them. So pallido-striate goes from the _____ to the _____.
pallido; globus pallidus; striatum
The globus pallidus and putamen together are referred to as as (lenticular nucleus or the lentiform nucleus/occular nucleus or the occulomotor nucleus). Lenticular and lentiform coming from the fact that when you look at them, they have a lens like shape to them. So that’s all. It just means they are a lens like structure that share a common function.
lenticular nucleus or the lentiform nucleus;
Ca – Caudate Put – putamen Thalamus – blue round circle GPe – Globus pallidus externus GPi – Globus pallidus internus
Globus Pallidus: control (conscious/unconscious) movement
(Internus/Externus): inhibits thalamus
(Internus/Externus): generally inhibits other portions of basal ganglia
If we break down, the connection’s a little bit more for the globus pallidus. So here we are looking front to back (pic on the left). So we are looking at the front of the caudate, putamen, and globus pallidus. Here we are looking at the thalamus and then a few other structures that we have not reviewed just yet, subthalamic nucleus and substantial Niagara (all the way at the bottom on the left). If we take a look at how the structures line up… So here we are looking at globus pallidus externus. When we take a look here, the globus pallidus externus is lined up fairly close to the (caudate/putamen). The globus pallidus externus’ inhibitory role is going to be within the (caudate/putamen) and a few other structures that are not shown here in this particular picture, specifically (cerebrum/nucleus accumbuns) and an area that we refer to as the (parkinsons area/ventral tegmental area). But the globus pallidus externus is setup to generally inhibit other portions of the basal ganglia because of where it sits between the _____ and the _____.
conscious; Internus; Externus; putamen; putamen; nucleus accumbuns; ventral tegmental area; putamen; caudate
The globus pallidus internus inhibits motion by having a general inhibitory role. So this is what’s pictured here (pic to the right). Globus pallidus internus sits right next to the _______, which is underneath the caudate. And so the globus pallidus internus has an overall inhibitory role on thalamic structures. If we think about everything that goes through the thalamus, by inhibiting the thalamus, you inhibit the structures that go through it, and in turn inhibit (vision/movement) from occurring. So again, there is a specificity of connection and geography that dictates the function of the globus pallidus externus and the globus pallidus internus.
thalamus; movement
Nucleus accumbens is a tricky one. It’s hard to picture and there aren’t really good pictures that I’ve found that illustrate the nucleus accumbens well, but it sits in there somewhere (pic all the way to the left). So we take a look at this picture here (pic to the top right), we have the putamen sitting here, the front end of the caudate, and then that round structure here in orange lighting up is nucleus accumbens. So it sits there-Ish. if we’re looking front-to-back, if we’re looking top to bottom, here is where the nucleus accumbens sits (pic to the bottom right). The nucleus accumbens is going to have a role in (speech production/learning). So we are going to leave that alone for now. But since we are going over all the anatomical structures of the basal ganglia and their geographic location. I figured I just put it in there for now. So we have a complete picture of the anatomical locations for these.
learning
Then we have the substantia nigra. It sits at the (mid-brain/hindbrain) level. The substantia nigra is referred to as such because it stains a very dark black color. The dark black staining comes from the heavy amount of (epinephrine/dopamine), which is a fairly major neurotransmitter for the basal ganglia system. So if we take a look at a cross section of the brainstem, here, we have the crus cerebri, which are corticospinal tracts descending down. We have the red nuclei and then we have the central aqueduct and the periaqueductal gray. The superior and inferior colliculi sitting right back here, across the midbrain. The substantia nigra sits right behind the crus ____. Think of what the crus cerebri is carrying. It contains our (motor/sensory) fibers. So there’s thought that, there might be some small, fine connections between the substantia nigra and the descending pathways (it hasn’t been validated yet). But the substantia nigra comes in two parts. There is a dark black compacted part, hence substantia nigra compacta, and then a wispy hair like part that we will call the substantia nigra reticularis. The (compacta/reticularis) is the dopamine releasing part of the substantia nigra and it results in modulation of basal ganglia structures. And the (compacta/reticularis) with its hair-like kind of tentacles coming out is responsible for output to the rest of the CNS. So compacta is within basal ganglia communication and reticularis, is remaining central nervous system communication.
mid-brain; dopamine; cerebri; motor; compacta; reticularis;
The ventral tegmental area (VTA) also plays a role in the basal ganglia. The VTA or ventral tegmental area is kind of (a separate/combined) structure and not part of the basal nucleus or the basal ganglia proper. It’s just the anterior portion of the tegmental area of the midbrain, which around the area of the blue arrow. The midbrain is separated into tectum and tegmentum. (Tectum/tegmentum) is the part that contains the superior and inferior colliculus. Everything else is referred to as the (tectum/tegmentum).
a separate; Tectum; tegmentum
Pathways that start with or end with “_____” are structures that are pathways that contain the substantia nigra. Ex: Nigro-striatal.
nigro
And then lastly, again, another kind of ambiguous structure, just like the nucleus accumbens, is a structure that is very important. It’s small and it’s embedded within (gray/white) matter, it’s the subthalamic nucleus. It sits underneath the thalamus and sits between the connection between the (cerebellum/cerebrum) and the brain ____. So here, if we’re looking here, we see the crus cerebri. We see the substantia nigra here, so that’s midbrain and then just right above the midbrain at the connection between the midbrain and the cerebrum is the subthalmic nuclei. What we’re looking at here is the internal capsule coming down into the crus cerebri. So those are the major structures of the basal nucleus/basal ganglia and their anatomical locations.
white; cerebrum; stem
The basal nucleus interacts with the cortex through (cerebellar/thalamic) relays. So there (is a/is no) connection, at least that we know of yet, between the basal nucleus and motor neurons. They are all indirect connections through thalamic relays.
thalamic; is no
So let’s review the cortical structures and the thalamic input to them. The first structure that we’ll deal with is the supplemental motor cortex. So supplemental cortex. What do I need you to know? It’s responsible for (afterward/preparatory) postural movements, (timing/vestibular), (sequencing/auditory), and (initiation/the end) of movement. The way it gets that information that it requires for timing, sequencing, and initiation of movement is through the (thalamus/cerebellum) to specific structures - The ventral anterior and the ventral lateral aspect of the thalamus. The ventral anterior aspect to the thalamus relays input from the (substantia nigra/subthalmic nucleus) and the (globus pallidus/nucleus accumbuns) to the supplemental motor cortex. The ventral lateral area relays information from the _____, (globus pallidus/nucleus accumbuns), and the (substantia nigra/subthalmic nucleus) to the supplemental motor cortex. So the anterior aspect takes info from substantia nigra & globus pallidus & passes it through. Information that’s coming from the ventral lateral is going to be influenced by the cerebellum, the globus pallidus, & the substantia nigra, all playing a role in the timing, sequencing and initiation of movement. Think of what the cerebellum does and consider why cerebellar information is important with respect to this particular activity that is happening within the supplemental motor cortex.
preparatory; timing; sequencing; initiation; thalamus; substantia nigra; globus pallidus; cerebellum; globus pallidus; substantia nigra;
The thalamus, which (is a/is not) part of the basal ganglia or basal nucleus, has a heavy connection with the basal nucleus. So we’re going to go over the ventral anterior, which from a geographic location sits right here. The two structures that are going to be playing with the basal nucleus in the thalamus are the ventral anterior and the ventral lateral nucleus. So the ventral anterior, which we talked about, having input to the supplemental cortex, also has projections to the (premotor/postmotor) area for planning of movement. It participates in the initiation and inhibition of (speech production/movement). So initiating wanted versus unwanted movements. It sits right at the bottom and (anterior/posterior) aspect of the thalamus.
is not; premotor; movement; anterior
We already know the VPL and the VPM in terms their role in the dorsal column-medial lemniscus and the anterolateral system as well as the descending tracks. The interesting thing about the ventral anterior and ventral lateral system is it also receives input from the ____ system, which is responsible for emotions. So we start to consider this idea of, do our emotions have an impact on movement? We’re also starting to see that the limbic system has an impact on (vision/learning). So the limbic system, if you guys recall, goes back to the cingulate gyrus where we were going over the cortices. Does the limbic system and its interconnections within the VA and the VL have a role in basal ganglia/basal nucleus mediated motor learning?
limbic; learning;
From a premotor cortex, we talked about the input that the premotor cortex is receiving from the ventral anterior. It also receives input from the ventral lateral aspect of the thalamus. The premotor cortex is responsible for association of (visual, auditory and somatosensory/tactile, language processing, & stereognosis) input and coordination of the movement of the (head, eyes and trunk/distal limbs). The premotor cortex receives input from the thalamus – ventral lateral and relays info from the (cerebrum/cerebellum) and (globus pallidus/substantia nigra) to the premotor cortex.
visual, auditory, and somatosensory; head, eyes, and trunk; cerebellum; globus pallidus;
The other pieces with respect to basal ganglia function are all the neurotransmitters that are involved. So there are three neurotransmitters that are agreed upon. Gaba has an overall (excitatory/inhibitory) role. Glutamate has an overall (excitatory/inhibitory) role. Then dopamine, which is a neurotransmitter is involved in motion, learning and reward and reinforcement of behavior does both. It excites and it inhibits, it really depends on the receptor that dopamine is attaching onto. DA1 receptors have an overall (excitatory/inhibitory) function and DA2 receptors have an overall (excitatory/inhibitory) function. So it depends on the structures and where those structures sit and the dopamine receptor representation at those particular structures that dictate whether dopamine is going to have an excitatory or inhibitory role.
inhibitory; excitatory; excitatory; inhibitory;
The basal nucleus and the thalamic relays play with the _____ cortex and the _____ cortex. It is through those two structures that is going to drive what happens at M1. Again, (there are/there aren’t) direct connections from the basal nucleus to M1/to motor neurons.
premotor; supplemental; there aren’t
Slide has 0 importance
So here we’re just looking at a frontal cut of the cortex and the basal ganglia structures
Got it
In general, the thalamus has an (inhibitory/excitatory) role on the cerebral cortex to the movement centers.
excitatory
The globus pallidus internus and the substantia nigra reticularis keep a constant (excitatory/inhibitory) signal. So here it is in red, to the thalamus to inhibit this (excitatory/inhibitory) signal. That inhibitory signal comes from the _____ nucleus, (exciting/inhibiting) the globus pallidus internus and the substantia nigra reticularis. So when the neurons of the globus pallidus internus go to potential, they release their gaba neurotransmitters, which are going to result in (inhibition/excitation). Similarly, when the neurons of the substantia nigra reticularis are excited, and go to potential, they release their neurotransmitters which are gabanergic resulting in (inhibition/excitation). So the overall result of the EPSP or the excitation at the subthalamic nucleus is to result in an (inhibitory/excitatory) signal being released from the globus pallidus internus and the substantia nigra reticularis onto the thalamic relays.
inhibitory; excitatory; subthalmic; exciting; inhibition; inhibition; inhibitory;
When the thalamic relays are inhibited, it’s going to result in the body staying (active/at rest) because this green excitatory signal from the thalamus (is/is not) getting to the cortical regions.
at rest; is not
But now we’re in a situation where we want to perform a movement, right? So there is a signal from the cortical drive that says, hey, I want to do something. That EPSP is going to travel down to the caudate and putamen. The putamen is going to play a (smaller/larger) role and caudate is going to play a (smaller/larger) role. But what’s going to happen is excitation from the cortex is going to result in EPSPs going down to the caudate and putamen, mostly putamen. What’s going to happen there then is the striatum is going to release an (EPSP or an excitatory/IPSP or an inhibitory) signal to the globus pallidus internus and the substantia nigra reticularis. So now the GP internus and the reticularis are not going to be able to send that (excitatory/inhibitory) signal to the thalamus anymore. And now the thalamus is free to do whatever it wants, resulting in (excitation/inhibition) of the cortical units responsible for movement. And therefore movement occurs. And so really that is the pathway for initiation of movement. There is an excitatory center, but at rest, inhibitory centers keep that excitatory center at bay. So then when we want movement, there is inhibition of the (excitatory/inhibitory) centers, which allows the excitatory centers to do their thing.
larger; smaller; IPSP or an inhibitory; inhibitory; excitation; inhibitory
So we’re going to go over the inhibition of unwanted movement. So it’s a simultaneous loop. So on the first side we’ve got the globus pallidus externus (exciting/inhibiting) the subthalamic nucleus. The subthalamic nucleus, has an (excitatory/inhibitory) function on the globus pallidus internus and the substantia nigra reticulata, resulting in (excitation/inhibition) of the thalamus. So if we have a globus pallidus externus inhibition of the subthalamic nucleus, the overall result is (excitation/inhibition) of the globus pallidus internus and substantia nigra reticularis. The thalamic inhibition is eliminated and the cortex is stimulated to (produce/inhibit) movement.
inhibiting; excitatory; inhibition; inhibition; produce;
When we want inhibition, what we have is information we’re signaling from the cortex that results in (inhibition/excitation) of the striatum (caudate, putamen, and MAYBE nucleus accumbens (it is still hotly debated on its’ role in this cycle) with (excitatory/inhibitory) signals going to the globus pallidus externus. When we have that, there’s also going to be a simultaneous signal that’s going to the subthalamic nucleus to create an (excitatory/inhibitory) signal. The subthalamic nucleus (excites/inhibits) globus pallidus internus and substantia nigra reticularis and the overall result is thalamic (excitation/inhibition). The cerebellar and cortical regions decide which parts it wants to inhibit. And then inhibition signal’s go to those specific regions of the thalamic relay. The overall end result is cerebral cortex (excitation/inhibition).
excitation; inhibitory; excitatory; excites; inhibition; inhibition
And really I want you to be aware of the nomenclature because from a clinical perspective and a pathological process, we refer to these two specific pathways. So yes, this is important for your clinical classes. So there are two pathways that we’re going to go over. The one is the direct pathway, which (inhibits/promotes) movement and then an indirect pathway which (inhibits/promotes) unwanted or excessive movements. So we’re talking about the tremulous behavior that James Parkinson described when we first started to introduce the basal ganglia.
promotes; inhibits
So the direct pathway is overseen by the substantia nigra pars (compacta/reticularis), which was that kind of circular structure sitting within the brainstem, midbrain. The substantia nigra pars compacta is going to release dopamine and it is going to be processed within the substantia nigra pars compacta and the globus pallidus (internus/externus). That dopamine is going to attach onto specific dA1 receptors. So those are the (excitatory/inhibitory) dopamine within the striatum. The excitation of the striatum is going to result in (excitation/inhibition) of the globus pallidus internus and the substantia nigra reticularis and it’s going to be pretty much everything that we talked about in terms of initiating movement. The end result is going to be that the thalamus is stimulated and movement is (promoted/inhibited). This is a slightly different pathway than the general pathway that we discussed. It’s this dysfunction of the nigrostriatal pathway and the (gain/loss) of the dopamine neurons that is attributed to the movement disorders that we see in Parkinson’s disease.
compacta; externus; excitatory; inhibition; promoted; loss
The indirect pathway (promotes/inhibits) excessive and erratic movements. The direct pathway and indirect pathway are working simultaneously to produce wanted and inhibit unwanted movements. It gets a little bit confusing because again, it’s substantia nigra pars (compacta/reticularis) that is playing a role in the indirect pathway as well and again, it has to do with dopamine. But what it is, is there are a different cluster of nuclei that dopamine is being attached to. So from a big picture perspective, the substantia nigra pars compacta is just releasing dopamine. Some of the dopamine attaches onto D1 receptors in nuclear clusters within the striatum to (inhibit/cause) movement and some of the dopamine is ending up on D2 receptors in different nuclear clusters to (cause/inhibit) unwanted movement. The end result really is that we (gain/lose) the inhibitory effect on the globus pallidus externus and we get further (excitation/inhibition) of the thalamus as an end result. It becomes relevant because these two pathways are the major pathways that become impacted with Parkinson’s disease.
inhibits; compacta; cause; inhibit; lose; inhibition;
