布鲁氏菌抗原试剂盒抗凝集血清群

布鲁氏菌抗原试剂盒抗凝集血清群

广州健仑生物科技有限公司

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布鲁氏菌抗原试剂盒抗凝集血清群

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【公司名称】 广州健仑生物科技有限公司
【市场部】    杨永汉

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【腾讯  】 
【公司地址】 广州清华科技园创新基地番禺石楼镇创启路63号二期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.

总结多巴胺  递质系统和乙酰胆碱递质系统的不同作用，目前认为黑质上行抵达纹  状体的多巴胺递质系统的功能，在于抑制纹状体内乙酰胆碱递质系统  的功能；震颤麻痹患者由于多巴胺递质系统功能受损，导致乙酰胆碱  递质系统功能的亢进，才出现一系列症状。如果应用左旋多巴以增强  多巴胺的合成，或应用M受体阻断剂以阻断乙酰胆碱的作用，均对震颤  麻痹有一定的治疗作用。静止性震颤的发生，可能与丘脑外侧腹核等  结构的异常活动有关。用微电极记录震颤麻痹患者丘脑外侧腹核的神  经元放电，可以观察到某些神经元具有周期性短串放电，其周期节律  与震颤肢体的节律相同步，破坏丘脑这些区域后则静止性震颤消失。  有人认为，这种异常活动是神经环路活动的结构结果，其通路可能为  ：丘脑外侧腹核→大脑皮层运动区→纹状体→丘脑外侧腹核。因为，  切断苍白球至丘脑外侧腹核的纤维后，也可使静止性震颤消失。  舞蹈病患者的主要临床表现为不自主的上肢和头部的舞蹈样动作，并  伴有肌张力降低等。病理研究证明，遗传性舞蹈病患者有显著的纹状  体神经元病变，新纹状体严重萎缩，而黑质-纹状体通路是完好的，脑  内多巴胺含量一般也正常。在这类患者，若采用左旋多巴进入治疗反  而使症状加剧，而用利血平耗竭包括多巴胺在内的神经递质，却可使  症状缓解。神经生化的研究发现，患者的纹状体中胆碱能神经元与γ-  氨基丁酸能神经元的功能明显减退。因此认为，舞蹈病病变主要是纹  状体内的胆碱能和γ-氨基丁酸能神经元功能减退，而黑质多巴胺能神  经元功能相对亢进，这和震颤麻痹的病变正好相反。目前知道，黑质  和纹状体之间有环路的；黑质的多巴胺能神经元的轴突上行抵达  纹状体，能控制纹状体内的胆碱能神经元的活动，转而改变纹状体内  γ-氨基丁酸能神经元的活动，然后γ-氨基丁酸能神经元的轴突下行  抵达黑质，反馈控制多巴胺能神经元的活动（图10-38）。当纹状体内  的胆碱能和γ-氨基丁酸能神经元病变时，上述环路功能受损，导致多  巴胺能神经元活动亢进。