What Is the Right Basal Ganglia?

The basal ganglia, also known as the basal nucleus, is the general term for the next large gray matter in the cerebral cortex. It is located in the deep white matter of the brain. It is mainly composed of the caudate nucleus, the bean-shaped nucleus, the screen-shaped nucleus, and the amygdala. In addition, the red nucleus, substantia nigra, and subthalamic nucleus also participate in the basal nucleus. The caudate nucleus and the lenticular nucleus are called striatum, and the lenticular nucleus is divided into two parts: the putamen and the pale bulb. ^[1]

Basal ganglia

The basal ganglia, also known as the basal nucleus, is the general term for the next large gray matter in the cerebral cortex. It is located in the deep white matter of the brain. It is mainly composed of the caudate nucleus, the bean-shaped nucleus, the screen-shaped nucleus, and the amygdala. In addition, the red nucleus, substantia nigra, and subthalamic nucleus also participate in the basal nucleus. The caudate nucleus and the lenticular nucleus are called striatum, and the lenticular nucleus is divided into two parts: the putamen and the pale bulb. ^[1]

Basal ganglia has important motor regulation functions. It is related to the stability of voluntary movement, the control of muscle tension, and the processing of proprioceptive information of proprioception, and participates in the formation of exquisite movement. When awake, recording the discharge activity of a single neuron in the pale globule, it was observed that the neuron activity significantly changed when the limbs performed voluntary movements; some neurons increased their discharge when the limbs flexed, indicating that the neurons in the bottom ganglia and Sports related. It has been observed in the animal experiments of electrical stimulation of the striatum that the stimulation of the striatum alone does not cause motor effects; however, if the cerebellar cortex is stimulated at the same time as the caudate nucleus or the pallidum is stimulated, the motor response of the cortex motor area That is to say, the inhibitory effect is rapid, and the inhibitory effect can continue for a certain period of time after the stimulation is stopped. In monkeys, the unilateral damage to the pale ball is not as convenient as the use of the lateral upper limbs. The above shows that the function of the basal ganglia is closely related to body movements, but these experimental facts still cannot explain how the basal ganglia regulates body movements.

Basal ganglia include the caudate nucleus, putamen and pale globules. The tail nucleus and the putamen are more advanced in evolution and have a functional relationship, collectively referred to as neostriatum. Pale spheres are older and are called old striatals. Also, the bottom

The clinical manifestations of basal ganglia damage can be divided into two categories:

Upper right: Schematic diagram of nigrostriatal loop

1: Dopaminergic neuron 2: Cholinergic neuron 3: -aminobutyric acid neuron 4: Striatum 5: Nigra dense part 6: Nigro reticulum

It has long been known that patients with tremor paralysis can be treated with M-type cholinergic receptor blockers (scopolamine, antan), indicating that the generation of tremor paralysis is also related to changes in the function of acetylcholine transmitters. In patients with tremor paralysis undergoing pale ball destruction surgery, if acetylcholine is directly injected into the pale ball, the symptoms of the contralateral limbs will be exacerbated, and the injection of M receptor blocker will decrease the symptoms. This shows that the acetylcholine transmitter system exists in the striatum, and the enhancement of its function will lead to the occurrence of tremor paralysis symptoms. Summarizing the different roles of the dopamine transmitter system and the acetylcholine transmitter system, it is currently believed that the function of the dopamine transmitter system that the nigra reaches the striatum is to inhibit the function of the acetylcholine transmitter system in the striatum; patients with tremor paralysis due to the dopamine transmitter The system function is impaired, leading to the hyperfunction of the acetylcholine transmitter system, and then a series of symptoms appear. If levodopa is used to enhance dopamine synthesis, or M receptor blockers are used to block the effects of acetylcholine, both have a certain therapeutic effect on tremor paralysis.

The occurrence of resting tremor may be related to abnormal activities of structures such as the lateral ventral nucleus of the thalamus. Using microelectrodes to record neuronal discharges in the lateral nucleus of the thalamus in patients with tremor palsy, it can be observed that some neurons have periodic short strings of discharges, the periodic rhythm of which is synchronized with the rhythm of the tremor limbs, and the tremor of the thalamus is destroyed after these areas are stopped disappear. Some people believe that this abnormal activity is the structural result of neural circuit activity, and its pathway may be: lateral ventral nucleus of thalamus motor area of cerebral cortex striatum lateral ventral nucleus of lateral thalamus. Because, after cutting the fiber connection between the pale globus and the lateral ventral nucleus of the thalamus, the resting tremor can also disappear.

The main clinical manifestations of chorea patients are involuntary dance-like movements of the upper limbs and head, accompanied by decreased muscle tone. Pathological studies have shown that patients with hereditary chorea have significant striatum neuronal lesions, severe neostriatum atrophy, the nigro-striatum pathway is intact, and dopamine levels in the brain are generally normal. In such patients, if levodopa is used for treatment, the symptoms will be exacerbated, and the depletion of neurotransmitters including dopamine with reserpine can relieve the symptoms. Neurochemical studies have found that cholinergic neurons and -aminobutyric energy neurons in the striatum of patients have significantly reduced function. Therefore, it is believed that cholinergic and -aminobutyric energy neurons are mainly decreased in the striatum, while dopaminergic neurons in the substantia nigra are relatively hyperactive, which is the exact opposite of tremor paralysis. It is currently known that there is a loop connection between the substantia nigra and the striatum; the axons of dopaminergic neurons in the substantia nigra reach the striatum, which can control the activity of cholinergic neurons in the striatum and change it. The activity of -aminobutyric energy neurons in the striatum, and then the axons of -aminobutyric energy neurons descend to the substantia nigra, which feedback controls the activity of dopaminergic neurons (Figure 10-38). When cholinergic and -aminobutyric energy neurons are damaged in the striatum, the above-mentioned loop function is impaired, resulting in hyperactivity of dopaminergic neurons.

Basal ganglia include the caudate nucleus, putamen nucleus, pale bulb, subthalamic nucleus, substantia nigra and red nucleus. The tail nucleus, putamen and pale globules are collectively called striatum. The striatum has the function of controlling muscle movements, and combines with the thalamus and hypothalamus to become the regulatory center of instinct reflexes, for example, to complete instinct reflexes such as walking.

When awake, recording the discharge activity of a single neuron of the pale globule, it was observed that the discharge of the neuron clearly changed when the limbs performed voluntary movements, indicating that the basal ganglia is related to voluntary movements. It has been observed in the animal experiments of electrical stimulation of the striatum that stimulating the striatum alone cannot cause motor effects; however, if the striatum is stimulated at the same time as stimulating the cerebral cortical motor area, the motor response from the cortical motor area will be affected. Suppresses quickly, and the inhibitory effect can persist for a certain time after the cessation of stimulation. The main manifestations of basal ganglia damage in clinic can be divided into two categories: one is a syndrome with too much exercise and muscular insufficiency (such as chorea), and the other is a syndrome with too little exercise and muscular tension Syndrome (such as tremor paralysis).

The symptoms of patients with tremor and palsy (Parkinson's disease) are: increased muscle tone throughout the body, muscle rigidity, reduced voluntary movements, slow movements, and dull facial expressions. In addition, patients are often accompanied by static tremor, which is more common in the upper limbs (especially the hands), followed by the lower limbs and the head; the tremor rhythm is about 4 to 6 times per second, which occurs at rest, and strengthens when emotionally excited. Reduced during voluntary exercise and stopped after falling asleep. The cause of tremor palsy has been well understood. In recent years, through the study of central neurotransmitters, it has been determined that the mesencephalic substantia nigra is the main site of dopaminergic neurons, and its fibers can reach the striatum (Figure 11-16). Pathological studies of patients with tremor palsy have demonstrated that the substantia nigra has lesions and that the dopamine content in the brain has decreased significantly. In animals, if catecholamines (including dopamine) are depleted with drugs (reserpine), the animal will experience symptoms similar to tremor paralysis; if further levodopa (precursor of dopamine) is given, it can enter the central nerve through the blood-brain barrier System) treatment, which increases dopamine synthesis in the body, then the symptoms ease. This shows that the destruction of dopaminergic neurons in the mesencephalic substantia nigra is the main cause of tremor paralysis.

It has long been known that patients with tremor paralysis can be treated with M-type cholinergic receptor blockers (scopolamine, diphenoxylate), indicating that the generation of tremor paralysis is also related to changes in the function of acetylcholine transmitters. In patients with palsy paralysis undergoing pale ball destruction surgery, if acetylcholine is directly injected into the pale ball, the symptoms of the contralateral limbs will be exacerbated, and the injection of M-type blockers will decrease the symptoms. This shows that the acetylcholine transmitter system exists in the striatum, and the enhancement of its function will lead to the occurrence of tremor paralysis symptoms. Summarizing the above research results, it is currently believed that the function of the dopamine transmitter system in the striatum is to inhibit the function of the acetylcholine transmitter system in the striatum. The patients with tremor and paralysis due to the impaired function of the dopamine transmitter system cause acetylcholine transmitter. A series of symptoms appear only when the function of the cytoplasmic system is hyperactive. If levodopa is used to enhance dopamine synthesis, or M-type blockers are used to block the effects of acetylcholine, tremor paralysis can be treated.

Under normal circumstances, the dopamine transmitter system that reaches the striatum in the substantia nigra is also associated with behavioral arousal. Animal experiments have observed that after simply destroying the mesencephalic dopamine transmitter system, animals cannot behave awakened in behavior, and can't express inquiry behavior to novel stimuli. The facial expression of patients with tremor paralysis may be a sign of behavioral disturbances.

The main clinical manifestations of chorea patients are involuntary dance-like movements of the upper limbs and head, accompanied by decreased muscle tone. Pathological studies have shown that the striatum is severely atrophied, and the nigro-striatum pathway is intact. In this group of patients, symptoms can be exacerbated if levodopa is used for treatment, while depletion of the dopamine transmitter with reserpine can relieve symptoms. Neurochemical studies have found that cholinergic neurons and -aminobutyric acid neurons in the striatum of patients have significantly reduced function. Therefore, it is believed that cholinergic and -aminobutyric energy neurons are mainly reduced in striatum, while dopaminergic neurons in substantia nigra are relatively hyperactive, which is exactly the opposite of the pathological mechanism of tremor paralysis. It is currently known that there is a loop connection between the substantia nigra and the striatum: the dopaminergic ascending system of the substantia nigra can inhibit the activities of the cholinergic and -aminobutyric acid systems in the striatum; The -aminobutyric acid descending system can feedback inhibit the activity of the dopaminergic system in substantia nigra (Figure 11-16). In the clinical treatment of tremor paralysis, if levodopa is used excessively, it can cause symptoms similar to chorea, which also shows that the above point is justified.