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甘丙肽是1983年发现的一种脑肠肽,与认知情感和内稳态的调节密切相关。本文着重综述了甘丙肽对多种学习记忆功能的抑制及调节学习记忆功能的机制:甘丙肽的过度表达破坏了学习记忆相关部位去甲肾上腺素、5-羟色胺和乙酰胆碱的平衡,使学习记忆功能处于病理状态;兴奋胆碱能M2突触前受体,反馈性减少乙酰胆碱释放;引起神经细胞膜超极化及外向性钾离子流,产生抑制性突触后电位,抑制乙酰胆碱释放;降低突触前膜兴奋性谷氨酸释放,损伤突触可塑性;甘丙肽受体是G蛋白偶联受体,甘丙肽在受体活化下游抑制腺苷酸化环化酶及转录因子CREB结合启动子,影响新的基因和蛋白表达,从而阻断短时记忆转入长时记忆。临床上在阿尔茨海默病和Down’s综合征等神经变性性疾病中,围绕Meynert基底核和斜角带核胆碱能神经元周围甘丙肽纤维和终末数量大大增加,提示使用甘丙肽拮抗剂治疗的可能。
Galanin, a brain gut peptide found in 1983, is closely related to the regulation of cognitive emotion and homeostasis. In this review, we summarize the inhibitory effects of galanin on many learning and memory functions and the mechanisms that regulate learning and memory. Overexpression of galanin disrupts the balance between norepinephrine, serotonin and acetylcholine in learning and memory-related sites, Memory function in the pathological state; excited cholinergic M2 presynaptic receptors, feedback to reduce the release of acetylcholine; cause neuronal membrane hyperpolarization and outward potassium current, inhibitory postsynaptic potential and inhibit the release of acetylcholine; Prenatal membrane excitatory glutamate release, damage synaptic plasticity; galanin receptor is a G protein-coupled receptor, galanin downstream of the receptor activation of adenylyl cyclase and transcription factor CREB binding promoter , Affecting new gene and protein expression, thus blocking short-term memory into long-term memory. Clinically, in neurodegenerative diseases such as Alzheimer’s disease and Down’s syndrome, the number of galanin fibers and terminals surrounding the basilar nucleus of Meynert and nuclei of chordal nuclei and cholinergic neurons have greatly increased, suggesting that galanin Antagonist treatment possible.