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廣州健侖生物科技有限公司

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【公司名稱】 廣州健侖生物科技有限公司
【市場部】    楊永漢

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【騰訊  】 
【公司地址】 廣州清華科技園創(chuàng)新基地番禺石樓鎮(zhèn)創(chuàng)啟路63號二期2幢101-103

Summarizing the different roles of the dopamine transmitter system and the acetylcholine transmitter system, it is currently believed that the function of the dopamine neurotransmitter system for the uptake of nigra up to the striatum is to inhibit the function of the acetylcholine transmitter system in the striatum; for patients with tremor paralysis due to the dopamine transmitter Impaired system function, resulting in hyperactivity of the acetylcholine transmitter system, a series of symptoms. If levodopa is used to enhance the synthesis of dopamine, or to use an M receptor blocker to block the effects of acetylcholine, it has a certain therapeutic effect on tremor paralysis. The occurrence of resting tremor may be related to the abnormal activity of the lateral ventral nucleus of the thalamus. Using microelectrode to record the neuronal discharge of the thalamic lateral ventral nucleus in paralytic paralyzed patients, we can observe that some neurons have periodical short bursts, and the periodic rhythm is synchronous with the rhythm of the limbs of the tremor, and the rest tremors after destroying these areas of the thalamus. disappear. Some people think that this abnormal activity is the structural result of neural circuit activity. The pathway may be: lateral thalamic nucleus → cerebral cortex motor area → striatum → lateral thalamic nucleus. Because, after cutting off the globus pallidus to the thalamic lateral ventral nucleus fiber connections, it can also make static tremor disappear. The main clinical manifestations of patients with chorea are involuntary dance-like movements of the upper limbs and head, accompanied by decreased muscle tone. Pathological studies have demonstrated that patients with hereditary chorea have significant striatum neuron lesions, severe striatum atrophy, and the nigra-striatum pathway is intact, and intracerebral dopamine levels are generally normal. In these patients, symptoms are exacerbated if levodopa is used to enter the treatment, and reserpine depletes neurotransmitters, including dopamine, to relieve symptoms. Neurochemical studies have shown that the function of cholinergic neurons and gamma-aminobutyric acid neurons in the striatum of patients is significantly reduced. Therefore, it is believed that the lesions of chorea are mainly cholinergic and gamma-aminobutyric acid neuronal dysfunction in the striatum, whereas the dopaminergic neurons of the substantia nigra are relatively hyperactive, which is the opposite of the palsy lesions. It is currently known that there is a looping link between the substantia nigra and the striatum; the axons of the substantia nigra dopaminergic neurons travel upstream to the striatum and can control the activity of the cholinergic neurons in the striatum and change. The activity of gamma-aminobutyric acid-producing neurons in the striatum, and then the axons of gamma-aminobutyric acid-producing neurons descend to the substantia nigra, feedback controlling the activity of dopaminergic neurons (Figure 10-38). When cholinergic and gamma-aminobutyric acid neurons in the striatum are damaged, the above loop function is impaired, resulting in hyperactivity of dopaminergic neurons.

總結多巴胺  遞質系統(tǒng)和乙酰膽堿遞質系統(tǒng)的不同作用，目前認為黑質上行抵達紋  狀體的多巴胺遞質系統(tǒng)的功能，在于抑制紋狀體內乙酰膽堿遞質系統(tǒng)  的功能；震顫麻痹患者由于多巴胺遞質系統(tǒng)功能受損，導致乙酰膽堿  遞質系統(tǒng)功能的亢進，才出現一系列癥狀。如果應用左旋多巴以增強  多巴胺的合成，或應用M受體阻斷劑以阻斷乙酰膽堿的作用，均對震顫  麻痹有一定的治療作用。靜止性震顫的發(fā)生，可能與丘腦外側腹核等  結構的異?；顒佑嘘P。用微電極記錄震顫麻痹患者丘腦外側腹核的神  經元放電，可以觀察到某些神經元具有周期性短串放電，其周期節(jié)律  與震顫肢體的節(jié)律相同步，破壞丘腦這些區(qū)域后則靜止性震顫消失。  有人認為，這種異?；顒邮巧窠洯h(huán)路活動的結構結果，其通路可能為  ：丘腦外側腹核→大腦皮層運動區(qū)→紋狀體→丘腦外側腹核。因為，  切斷蒼白球至丘腦外側腹核的纖維后，也可使靜止性震顫消失。  舞蹈病患者的主要臨床表現為不自主的上肢和頭部的舞蹈樣動作，并  伴有肌張力降低等。病理研究證明，遺傳性舞蹈病患者有顯著的紋狀  體神經元病變，新紋狀體嚴重萎縮，而黑質-紋狀體通路是完好的，腦  內多巴胺含量一般也正常。在這類患者，若采用左旋多巴進入治療反  而使癥狀加劇，而用利血平耗竭包括多巴胺在內的神經遞質，卻可使  癥狀緩解。神經生化的研究發(fā)現，患者的紋狀體中膽堿能神經元與γ-  氨基丁酸能神經元的功能明顯減退。因此認為，舞蹈病病變主要是紋  狀體內的膽堿能和γ-氨基丁酸能神經元功能減退，而黑質多巴胺能神  經元功能相對亢進，這和震顫麻痹的病變正好相反。目前知道，黑質  和紋狀體之間有環(huán)路的；黑質的多巴胺能神經元的軸突上行抵達  紋狀體，能控制紋狀體內的膽堿能神經元的活動，轉而改變紋狀體內  γ-氨基丁酸能神經元的活動，然后γ-氨基丁酸能神經元的軸突下行  抵達黑質，反饋控制多巴胺能神經元的活動（圖10-38）。當紋狀體內  的膽堿能和γ-氨基丁酸能神經元病變時，上述環(huán)路功能受損，導致多  巴胺能神經元活動亢進。