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Effects of the Aconitum alkaloid songorine on synaptic transmission and paired-pulse facilitation of CA1 pyramidal cells in rat hippocampal slices

机译:乌头碱生物碱对大鼠海马切片CA1锥体细胞突触传递和成对促进的影响

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class="enumerated" style="list-style-type:decimal">The present study investigated the electrophysiological effects of songorine (1–100 μM), an alkaloid occurring in plants of the Aconitum genus, in rat hippocampal slices.Songorine (10–100 μM) evoked a concentration-dependent increase in the amplitude of the orthodromic population spike and in the slope of the field e.p.s.p. The enhancement was long-lasting and was not reversed by up to 90 min of washout. Songorine failed to affect size and shape of the presynaptic fiber spike which represents the compound action potential of the Schaffer collaterals. This indicates that enhancement of the synaptic response is no consequence of an increased afferent excitability.The antidromically evoked population spike was not affected by songorine at concentrations up to 100 μM suggesting that the enhancement of the orthodromic population spike and of the field e.p.s.p. was not due to an increase in pyramidal cell excitability.The input-output curve for the postsynaptic population spike was shifted to the left implying that a presynaptic fiber spike of the same size elicited a larger postsynaptic response, indicating a decrease in threshold for generation of the population spike.The songorine-evoked increase in excitability was not affected by the NMDA receptor antagonist, D-AP5. However, the effect of songorine was completely abolished by the selective dopamine D2 receptor antagonist sulpiride (0.1 μM) as well as by haloperidol (10 μM) and was mimicked by application of the dopamine releaser, amantadine (100 mM). In contrast, the selective D1 receptor antagonist, , did not block the action of songorine.The results indicate that the plant alkaloid songorine enhances excitatory synaptic transmission which may be due to an agonistic action at D2 receptors.
机译:class =“ enumerated” style =“ list-style-type:decimal”> <!-list-behavior =枚举前缀-word = mark-type = decimal max-label-size = 0-> 本研究调查了松鼠碱(1–100μM),一种在乌头属植物中存在的生物碱,在大鼠海马切片中的电生理作用。 松鼠碱(10–100μM)引起了浓度依赖性矫正性种群峰值的幅度和场epsp的斜率增加增强效果是持久的,并且直到90分钟的冲洗时间都不会逆转。 Songorine不能影响突触前纤维刺的大小和形状,这代表了Schaffer侧支的复合动作电位。这表明突触反应的增强不是传入兴奋性增加的结果。 抗溴化诱发的种群峰值在浓度高达100μM的条件下不受松果氨酸的影响,这表明正畸种群的峰值和epsp的领域并不是由于锥体细胞兴奋性的增加。 突触后种群尖峰的输入-输出曲线向左移动,这意味着相同大小的突触前纤维尖峰会引起更大的突触后反应,表明 NMDA受体拮抗剂D-AP5不会影响松果碱引起的兴奋性增加。但是,选择性多巴胺D2受体拮抗剂舒必利(0.1μm)和氟哌啶醇(10μm)完全消除了松花碱的作用,而应用多巴胺释放剂金刚烷胺(100μmM)则模仿了松鸟碱的作用。相比之下,选择性D1受体拮抗剂不会阻断松香碱的作用。 结果表明,植物生物碱松香碱可增强兴奋性突触传递,这可能是由于对D2受体的激动作用所致。 / li>

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