突触间隙

乙酰胆碱酯酶（AChE）是与突触体相关联的一种蛋白酶，可促进神经递质乙酰胆碱在胆碱能突触间隙的水解。

AChE is a protein closely correlative with synaptosome . The hydrolysis of neurotransmitter-acetylcholine in the cholinergic synaptic cleft was regulated by AChE .

应激还影响大鼠海马Glu摄取，使高水平Glu在突触间隙内的存留时间延长，出现兴奋毒性的可能性增大；

Glutamate uptake of hippocampus was also affected by stress which lead to prolonged high level of Glu in synaptic cleft .

扫描电镜观察5s组次级突触间隙呈正常状态；

The secondary synaptic space was in normal state in 5 s group ;

轴棘、轴树突触间隙宽度变窄（P0.01），突触小泡数量减少（P0.01）。

The amount of synaptic vesicles showed fewer and the axo & spine and the axo-dendritic width narrow . The statistical differences were significant ( P0.01 ) .

压榨15s和30s组，口肌初级突触间隙接近正常。

M. oscular primary synaptic cleft was near to normal in groups 15 s and 30 s.

并且在消退训练后21d，消退组突触间隙宽度显著低于消退对照组（p0.05）。

At 21d , the width of synaptic gap was significantly lower in extinction group than that in the control group ( p0.05 ) .

依赖Na/Cl的GABA转运蛋白对控制GABA在突触间隙中的浓度起到重要作用，并因此而控制了GABA在突触传递中的强度和持续时间。

Na / Cl - dependent GABA transporters play an important role in controlling the concentration of GABA in the synaptic cleft , and thus they control the intensity and duration of synaptic transmission of GABA .

结论异丙酚以非竞争性的方式抑制了DAT的转运功能，降低了多巴胺（DA）的再摄取，导致突触间隙DA浓度升高，从而增强了中枢多巴胺能神经信息的传递。

Conclusion Propofol inhibits the transport ability of DAT in a noncompetitive fashion and reduces the reuptake of dopamine , leading to elevation in DA concentration in the synaptic cleft and potentiation of dopaminergic neurotransmission in central nervous system .

之后为了停止讯号的传送，VTA神经元会收回突触间隙的多巴胺，并重新组装以备再度需要的时刻。

To later shut down the signal , the VTA neuron removes the dopamine from the synaptic cleft and repackages it to be used again as needed .

当神经末梢胞浆中游离的NE浓度过高时，会反馈抑制囊泡中NE的生物合成，当冲动到达神经末梢时，NE释放到突触间隙减少，功能降低，从而引起抑郁的产生。

When the nerve endings of the NE concentration is too high , it will feedback and inhibit biosynthesis of NE vesicles . When the impulse reaches the nerve endings , NE released into the synaptic will decrease , which led to the emergence of depression .

以往的研究多侧重于突触前和突触间隙调节机制，而对突触后调节机制研究不多。

In the past , study of postsynaptic regulatory mechanism is rare .

尚可见锌离子存在于突触间隙内。

Moreover , free zinc ions could be found in the synaptic cleft .

实验性面瘫面肌次级突触间隙结构变化的电镜观察

Observation of Structural Difference of Secondary Synaptic Space of Facial Muscle in Facial Paralysis

然而，谷氨酸在突触间隙的过度聚集可引起神经元损伤甚至死亡，被称为兴奋性神经毒。

However , excessive accumulation of glutamate at synaptic clefts would cause neuronal damage even cell death , which is called excitotoxicity .

15s1周组的次级突触间隙面积轻度减少，1月组明显恢复；

The area of the secondary synaptic space decreased slightly in 15 s 1 week group but restored evidently in 1 month group ;

扫描电镜观察各1周组、1月组口轮匝肌次级突触间隙面积的变化。

The change of the secondary synaptic space area of musculus orbicularis oris in 1 week and 1 month group was observed via scanning electron microscope .

方法应用扫描电镜观察眼肌和口肌运动终板次级突触间隙的病理变化差异。

Methods The differences in pathological changes of secondary synaptic space of motor end plate of orbicularis oculi and oris muscles were observed under scanning electron microscope .

目的：探讨面神经麻痹面肌运动点的兴奋性与运动终板次级突触间隙的关系。

Objective : Our purpose was to study the relationship between the excitability of facial muscular motor point and the secondary synaptic space of motor terminal plate in facial paralysis .

结论由于眼肌次级突触间隙比口肌次级突触间隙受伤程度重，决定了两肌间受伤差异，支持了面肌程度判定的局部评价系统的合理性。

Conclusion Since injury degree of secondary synaptic space of orbicularis oculi muscles was more severe than that of oris muscles , it determined the differences in vulnerability and supported the local estimating system .

谷氨酸由内毛细胞释放到突触间隙中，被支持细胞膜上的谷氨酸&天冬氨酸转运体转运进入支持细胞，在谷氨酰胺合成酶作用下转变为谷氨酰胺并被释放到细胞外。

Glutamate is released from the inner hair cells , and taken up by supporting cells through the glutamate transporter ( GLAST ) . Glutamate is converted to glutamine ( Gln ) by glutamine synthetase ( GS ) and then transferred to inner hair cells .

突触界面曲率、突触间隙宽度、突触后致密物厚度均减小。

Moreover , the curvature of synaptic interface , the width of synaptic cleft and the thickness of post synaptic density were decreased .

突触前膜、突触后膜和突触间隙清晰，突触前终末有较多清亮的圆形囊泡，突触后膜有电子密度高的致密物质。

Presynaptic membrane , postsynaptic membrane and synaptic cleft were clear . Presynaptic terminals had more round clearest vesicles , and postsynaptic membrane has a high density electron . 3 .

阿片受体阻滞剂纳洛酮能够改善这种损害，其神经机制并非是增加ChAT活性，而是能促进神经元突触囊泡Ach向突触间隙大量释放，及增加突触后致密物质密度。

The neuromechanism may not enhance ChAT expression quality , but augmentation Ach exocytosis and post-synaptic density .

SAH14d组突触活性区长度、突触间隙宽度、PSD厚度较正常对照组大鼠减少，差异有统计学意义（p0.05）。

Synaptic active zone length , the width of synaptic cleft and PSD thickness were significantly less in SAH 14d group than in controls ( p0.05 ) . 4 .

超微结构的改变：SHR大脑皮质内神经元随着血压的升高出现核固缩、线粒体肿胀、嵴消失以及突触前后膜肿胀、突触间隙消失等改变。

Changes of the ultrastructure : The neurons in the cortex of SHR with the ascending of blood pressure , appeared karyopyknosis , mitochondria swollen , crista lost , the membranes of pre-synaptic and post-synaptic were not clear and the synaptic space was disappeared .

结果：突触界面曲率减小，突触间隙宽度加大，突触后膜致密物质厚度明显变薄，穿孔性突触的比例也有不同程度降低。

Results : The thickness of postsynaptic density material , the curvature of synaptic interface and the occurrence of perforated synapses decreased , while the width of synaptic cleft increased .

电镜显示：烫伤以后脑毛细血管周围出现空泡化，内皮肿胀，基底膜厚薄不均，星形胶质细胞足突空泡化。突触数量及突触小泡减少，突触间隙增宽。

In addition , vacuolated , swollen endothelium , abnormity of capillary basement membranes of BBB , marked vacuolar degeneration of the end feet of astrocytes , decreased number of synapse , synapse vesicle and broaden synaptic cleft were observed with transmission electron microscope .

结果表明：饮用高浓度氟化钠溶液能显著降低小鼠的学习能力，并能引起小鼠海马CA3区突触后致密物质厚度极显著减小，和引起突触间隙宽度极显著变大等超微结构的变化。

The main results are as follows : the learning ability of mice drinking high concentration of fluoride presented remarkable deterioration , the thickness of post synaptic density ( PSD ) was decreased , and the width of synaptic cleft was remarkably increased .

而在经过强化的突触这里，传递信息的细胞会释放更多谷氨酸到突触间隙，接受信息的细胞也可能会更有效率地结合谷氨酸。

In a strengthened synapse , the informing cell releases more glutamate into the synaptic gap and / or the informed cell is more efficient at binding the glutamate .