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锌是人体内含量仅次于铁的微量元素 ,在哺乳动物脑组织中浓度非常高 ,并以囊泡形式存在于突触前终末。神经细胞兴奋时可导致突触 Zn2 + 释放 ,它对突触传递可能起着调节作用。许多证据表明 ,突触 Zn2 + 过多释放导致突触后神经元内 Zn2 + 大量聚集 ,可能与某些急性脑疾患 (包括癫痫发作和暂时性全脑缺血 )并发的神经元损伤有关。由此推测 ,Zn2 + 内稳态的丧失可能与一些退化性疾病有关系 ,如老年性痴呆。进一步阐明 Zn2 + 在脑内的病理作用将有助于指导上述疾病的治疗
Zinc is second only to iron in the human body trace elements in mammalian brain tissue concentrations are very high, and the presence of vesicles in the pre-synaptic terminal. Excitability of nerve cells can lead to the release of synaptic Zn2 +, which may play a regulatory role in synaptic transmission. Much evidence suggests that excessive Zn2 + release from synapses leads to massive accumulation of Zn2 + in postsynaptic neurons and may be associated with neuronal damage associated with some acute brain disorders, including seizures and transient global cerebral ischemia. It is speculated that the loss of Zn2 + homeostasis may be associated with some degenerative diseases, such as Alzheimer’s disease. To further clarify the pathological role of Zn2 in the brain will help guide the treatment of these diseases