β-amyloid peptide25-35 depresses excitatory synaptic transmission in the rat basolateral amygdala "in vitro"
β-amyloid peptide25-35 depresses excitatory synaptic transmission in the rat basolateral amygdala "in vitro"
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DOI：
10.1016/j.neurobiolaging.2004.05.008
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发表时间：
2005-04-01
影响因子：
4.2
通讯作者：
Yajeya, J
中科院分区：
文献类型：
--
作者：
Ashenafi, S;Fuente, A;Yajeya, J
在成年大鼠脑片上观察了β-淀粉样肽（25-35）对基底外侧杏仁复合体静息膜电位、自发和诱发动作电位及突触活动的影响。细胞内记录显示，以400 nM或更低浓度灌注β-淀粉样肽（25-35）对静息膜电位没有产生任何影响。然而，在800-1200 nM范围内的浓度产生不可预测的作用，去极化和/或超极化，其被河豚毒素或6-氰基-7-硝基喹喔啉-2，3-二酮+ D-（-）-2-氨基-5-膦酰基戊酸与荷包牡丹碱一起阻断。灌流β-淀粉样肽25 -35后，谷氨酸或γ-氨基丁酸介导的兴奋性和抑制性诱发反应的幅度降低。此外，使用配对脉冲协议获得的结果提供支持突触前的作用方式，以确定哪种类型的受体和/或通道参与突触前的作用机制，α-7烟碱受体的特异性阻滞剂（甲基caconitine柠檬酸盐）或L-型钙通道阻滞剂（calcicludine或硝苯地平）被使用。β-淀粉样肽（25-35）在对照条件下以及在用甲基甘草次酸盐永久灌注的切片中降低兴奋性突触后电位幅度。然而，这种作用被阻断在切片灌注calcicludine或硝苯地平表明参与的L-型钙通道。总的来说，这些实验提供了β-淀粉样肽（25-35）影响基底外侧杏仁核中的神经传递的证据，并且其作用是通过L-型钙通道介导的。(C)2004爱思唯尔公司All rights reserved.
The effects of beta-amyloid peptide(25-35) on resting membrane potential, spontaneous and evoked action potential and synaptic activity have been studied in basolateral amygdaloid complex on slices obtained from adult rats. Intracellular recordings reveal that perfusion with beta-amyloid peptide(25-35) at concentrations of 400 nM and less did not generate any effect on resting membrane potential. However, concentrations in the range of 800-1200 nM produced an unpredictable effect, depolarization and/or hyperpolarization, which were blocked by tetrodotoxin or 6-cyano-7-nitroquinoxaline-2,3-dione + D-(-)-2-amino-5-phosphonopentanoic acid together with bicuculline. Excitatory and inhibitory evoked responses mediated by glutamic acid or gamma-aminobutyric acid decreased in amplitude after beta-amyloid peptide25-35 perfusion. Additionally, results obtained using the paired-pulse protocol offer support for a presynaptic mode of action.To determine which type of receptors and/or channels are involved in the presynaptic mechanism of action, a specific blocker of alpha-7 nicotinic receptors (methyllycaconitine citrate) or L-type calcium channel blockers (calcicludine or nifedipine) were used. beta-amyloid petide(25-35) decreased excitatory postsynaptic potentials amplitude in control conditions and also in slices permanently perfused with methyllycaconitine citrate. However, this effect was blocked in slices perfused with calcicludine or nifedipine suggesting the involvement of the L-type calcium channels. On the whole, these experiments provide evidence that beta-amyloid peptide(25-35) affects neurotransmission in basolateral amygdala and its action is mediated through L-type calcium channels. (C) 2004 Elsevier Inc. All rights reserved.