 Basal ganglia as the nail indicates is a group of nuclei located at the base of the brain. So, what are these nuclei? These are caudate nucleus, putamen, globus pallidus, substantia nigra pass reticulata and subthalamic nucleus. So, these five nuclei form the basal ganglia. Now, among these caudate nucleus and putamen together are known as striatum. Now, this striatum acts as a receiving nuclei of basal ganglia. That is, striatum receives the afferents which are coming through the basal ganglia. While, globus pallidus and substantia nigra pass reticulata are the output nuclei. That means they send the efferents from the basal ganglia. And subthalamic nuclei is connected to the globus pallidus. Now, let us elaborate on that basic circuitry. Palamic trigger, exciting the cortex and palimus send the negative control of basal ganglia. So, instead of basal ganglia, now we will introduce the receiving and output nuclei of basal ganglia. So, instead of basal ganglia, let us write here striatum and globus pallidum. Since, globus pallidus is the output nuclei of the basal ganglia. So, that means globus pallidus will send the inhibitory signal to the palimus. So, here it will be globus pallidus. Now, this striatum receives signals either from cortex or from substantia nigra pass compacta which causes release of dopamine. For simplicity sake, we are writing here only as cortex. But actually, this striatum receives input from vast areas of the cortex. So, there are various loops connecting different regions of the cortex to basal ganglia and palimus. So, one of these loops is the motor loop, where motor cortex has connections with the striatum. The striatum has connections with globus pallidus, palimus and again back to the cortex. Then, there are other loops also which is non-motor loops. This is there the basal ganglia has connections with the singulate cortex. So, this will be responsible for the limbic and emotional functions. So, like the movement for the facial expressions, the expression of emotions. So, these non-motor loops are the ones which control that limbic and emotional functions. Then, there is another ocular motor loop also for control of the eye movement. However, we are splitting these into loops, but you see the main activity of basal ganglia and all the loops will be to modulate the thalamocortical activity. That is, either for the initiation of motor activity or for the suppression of motor activity. So, when initiation of any motor activity is needed, we will want that this inhibitory control of the basal ganglia to the thalamus should be withdrawn, so that thalamus is able to stimulate the cortex. For suppression of motor activity, we will need that this inhibitory control of the basal ganglia to the thalamus is retained or maybe even made stronger and thalamus is not able to excite the cortex. Now, this is a schematic diagram of basal ganglia nuclei showing this tritum, pallidum as two parts, globus pallidus externa and globus pallidus interna. We were telling that pallidus inhibits the thalamus. So, here that internal part of the pallidus that is the globus pallidus internus actually keeps the thalamus inhibited. Then, we know that excitatory signals from thalamus go to the cortex. Now, we will introduce some other components also. So, apart from GPi, there is another nucleus that is the substantia nigra pas reticulose, which also keeps thalamus inhibited. Now, in direct pathway, the stricter neurons have an inhibitory control over neurons of GPi. Because the stricter is directly inhibiting the output nuclei of basal ganglia, that is why this is known as the direct pathway. It also inhibits substantia nigra pas reticulose. But remember, these stricter neurons do not fire tonically. Only when they are activated, they will burst inhibition. Tonic firing occurs in GPi and Snvr. Okay, now let us see the indirect pathway. In indirect pathway, two more nuclei come into hold. That is the GPi and subthalamic nucleus. So, in indirect pathway, stricter inhibits GPi, which in turn inhibits GPi. So, if you see what is happening, that stricter is actually exciting GPi. In direct pathway, what happened? That stricter was inhibiting GPi so that GPi won't be able to inhibit thalamus. That means the thalamus was becoming disinhibited. Here, GPi is actually inhibiting GPi. But if GPi is inhibited by stricter, it will not be able to inhibit GPi and GPi will continuously keep on inhibiting thalamus. Another nucleus which has a role in indirect pathway is subthalamic nucleus. Subthalamic nucleus has an excitatory connection with globus pallidus in turnus. So, that means when subthalamic nucleus is active, globus pallidus will be able to inhibit thalamus more. But subthalamic nucleus is itself inhibited by globus pallidus in turnus. So, basically in indirect pathway, this GPi, globus pallidus in turnus, is inhibiting globus pallidus in turnus by two ways. First, by directly inhibiting globus pallidus in turnus and secondly, preventing the excitation of GPi from subthalamic nucleus by inhibiting subthalamic nucleus. Let's summarize what we have understood till now. First of all, for movement to be initiated, thalamus should excite cortical neurons. For this, GPi should be inhibited since GPi is tonically inhibiting thalamus. Only when GPi is inhibited, thalamus will be disinhibited and it will be able to excite the cortex. Secondly, we saw that stricter neurons are not always active. But when they are active, they can act by two pathways, direct and indirect. Now, the fundamentals. You see the direct pathway when it is active, it facilitates movement. And when indirect pathway is active, it inhibits movement. How? Indirect pathway? Because stricter is inhibiting GPi, GPi will not be able to inhibit thalamus. Thus, thalamus can send excitatory signals to cortex. So, thalamus is triggering cortex for movement. So, indirect pathway is facilitated movement. On the other hand, indirect pathway, if you solve all these connections, what will happen? That ultimately, it will cause GPi to be able to inhibit thalamus more. So that, thalamus will not be able to excite cortex. So, indirect pathways inhibiting movement. So, how can the movement be initiated? Now, this direct and indirect pathway which we saw exists for each and every movement. Say for example, if you want to flex your arm. So, there is one direct pathway and one indirect pathway for your elbow flexion. So, direct pathway will facilitate elbow flexion and indirect pathway will inhibit elbow flexion. Similarly, for elbow extension, there is direct pathway and also an indirect pathway. Direct pathway facilitates elbow extension and indirect pathway inhibits elbow extension. So, if you want to flex your elbow, what happens? The direct pathway of elbow flexion is activated so that there is facilitation of elbow flexion and indirect pathway of elbow extension is activated so that there is inhibition of elbow extension. As we have said here, direct pathway facilitates movement, indirect pathway inhibits movement. So, for successful elbow flexion to occur, direct pathway of this movement is activated and indirect pathway of opposite movement is inhibited. But what about indirect pathway of elbow flexion? If that is also activated, then even if there is activation of the direct pathway, indirect pathway will tend to suppress that movement. So, there will be hesitation or trouble in initiating the movement. Because, indirect pathway is kind of putting a break on that point. So, here comes the role of dopamine released from substantial micro-pass compactor. Neurons from substantial micro-pass compactor have connections with the striator. These neurons release dopamine which act on a striator neurons in a differential manner. The released dopamine cites the direct pathway but it inhibits the indirect pathway. So, since direct pathway facilitates movement, its excitation facilitates the movement. And since indirect pathway inhibits movement, dopamine inhibits indirect pathway and thus facilitating the movement. So, this dopamine is said to have a modulated tree role for the movement. Because cortex itself is able to initiate the movement. However, indirect pathway will put a break on it. But dopamine will facilitate the movement and there will be no hesitation in initiating the movement. Problems in this circuitry will create movement disorders. Either there will be disorders in initiation of motor activity or disorders in suppression of motor activity. If flobus pallidus does not inhibit thalamus when required, it will lead to increased excitatory signal from thalamus to the cortex. This will happen because flobus pallidus is not able to inhibit thalamus. So, this increased trigger will lead to hyperkinetic disorders. On the other hand, if pallidum suppresses too much, that means this inhibitory signal becomes too strong, there will be decreased excitation of cortex from the thalamus. So, this green signal will be lesser and it will lead to some hypokinetic disorders because cortex is less excited. So, with basal ganglia disorders, there can be movement disorders of both types in which there is a problem in initiation of motor activity which are known as the hyperkinetic disorders and there may be problems in suppression of motor activity which are known as the hyperkinetic disorders.