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Effect of caffeine on long-term potentiation-like effects induced by quadripulse transcranial magnetic stimulation

机译:咖啡因对四颅颅磁刺激诱导的长期增强效果的影响

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Caffeine, an adenosine receptor antagonist, is known to affect sleep-awake cycles, the stress response, and learning and memory. It has been suggested that caffeine influences synaptic plasticity, but the effects of caffeine on synaptic plasticity in the human brain remain unexplored. The present study aimed to investigate the effects of caffeine on long-term potentiation (LTP)-like effects in the primary motor cortex of healthy humans. Twelve healthy participants (six women and six men; mean age: 44.8 +/- 1.5years) underwent quadripulse magnetic stimulation with an inter-stimulus interval of 5ms (QPS5) to induce LTP-like effects, 2h after administration of either a caffeine (200mg) or placebo tablet in a double-blind crossover design. We recorded motor-evoked potentials (MEPs) before and after QPS5. The degree of MEP enhancement was compared between the placebo and caffeine conditions. Neither active nor resting motor thresholds were influenced by caffeine administration. Following caffeine administration, the degree of potentiation significantly decreased in significant responders, whose average MEP ratios were greater than 1.24 in the placebo condition. The observed reduction in potentiation following caffeine administration is consistent with the A(2A) receptor antagonistic effect of caffeine. This is the first report of an effect of caffeine on neural synaptic plasticity in the human brain, which is consistent with the caffeine-induced plasticity reduction observed in primate studies. Because we studied only a small number of subjects, we cannot firmly conclude that caffeine reduces LTP in humans. The present results will, however, be helpful when considering further or new clinical uses of caffeine.
机译:咖啡因是一种腺苷受体拮抗剂,已知影响睡眠唤醒循环,应力响应和学习和记忆。已经提出咖啡因影响突触可塑性,但咖啡因对人脑中突触可塑性的影响仍未探索。本研究旨在探讨咖啡因对健康人类初级运动皮层中长期增强(LTP)的影响。十二名健康参与者(六名妇女和六名男性;意思是年龄:44.8 +/- 1.5°)通过5ms(QPS5)的刺激间隔进行四态磁刺激,以诱导LTP样效果,施用咖啡因后2小时( 200毫克)或安慰剂片中的双盲交叉设计。在QPS5之前和之后,我们记录了电动诱发的电位(MEP)。在安慰剂和咖啡因条件之间比较了MEP增强程度。无论是活跃还是休息的电机阈值都没有受到咖啡因给药的影响。在咖啡因管理后,显着响应者的增强程度显着降低,其平均MEP比率在安慰剂条件下大于1.24。观察到的咖啡因给药后的增强性与咖啡因的A(2A)受体拮抗作用一致。这是咖啡因对人脑中神经突触塑性作用的第一报告,这与灵长类动物研究中观察到的咖啡因诱导的可塑性减少一致。因为我们只研究了少数科目,我们不能坚决得出结论咖啡因在人类中减少了LTP。然而,目前的结果将在考虑进一步或新的临床用途时有助于咖啡因。

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