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首页> 外文期刊>Journal of Neurophysiology >Short-term plasticity at inhibitory synapses in rat striatum and its effects on striatal output.
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Short-term plasticity at inhibitory synapses in rat striatum and its effects on striatal output.

机译:大鼠纹状体抑制突触的短期可塑性及其对纹状体输出的影响。

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Two forms of short-term plasticity at inhibitory synapses were investigated in adult rat striatal brain slices using intracellular recordings. Intrastriatal stimulation in the presence of the ionotropic glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (20 microM) and D,L-2-amino-5-phosphonovaleric acid (50 microM) produced an inhibitory postsynaptic potential (IPSP) that reversed polarity at -76 +/- 1 (SE) mV and was sensitive to bicuculline (30 microM). The IPSP rectified at hyperpolarized membrane potentials due in part to activation of K(+) channels. The IPSP exhibited two forms of short-term plasticity, paired-pulse depression (PPD) and synaptic augmentation. PPD lasted for several seconds and was greatest at interstimulus intervals (ISIs) of several hundred milliseconds, reducing the IPSP to 80 +/- 2% of its control amplitude at an ISI of 200 ms. Augmentation of the IPSP, elicited by a conditioning train of 15 stimuli applied at 20 Hz, was 119 +/- 1% of control when sampled 2 s after the conditioning train. Augmentation decayed with a time constant of 10 s. We tested if PPD and augmentation modify the ability of the IPSP to prevent the generation of action potentials. A train of action potentials triggered by a depolarizing current injection of constant amplitude could be interrupted by stimulation of an IPSP. If this IPSP was the second in a pair of IPSPs, it was less effective in blocking spikes due to PPD. By contrast, augmented IPSPs were more effective in blocking spikes. The same results were achieved when action potentials were triggered by a depolarizing current injection of varying amplitude, a manipulation that produces nearly identical spike times from trial to trial and approximates the in vivo behavior of these neurons. These results demonstrate that short-term plasticity of inhibition can modify the output of the striatum and thus may be an important component of information processing during behaviors that involve the striatum.
机译:使用细胞内记录在成年大鼠纹状体脑切片中研究了两种形式的抑制突触的短期可塑性。在离子型谷氨酸受体拮抗剂6-氰基-7-硝基喹喔啉-2,3-二酮(20 microM)和D,L-2-氨基-5-膦酰戊酸(50 microM)存在下的纹状体内刺激产生抑制性突触后电位(IPSP),其极性在-76 +/- 1(SE)mV时反转,并且对双小分子(30 microM)敏感。 IPSP在超极化膜电势下整流,部分原因是激活了K(+)通道。 IPSP表现出短期可塑性的两种形式,成对脉冲抑制(PPD)和突触增强。 PPD持续几秒钟,并且在数百毫秒的激励间隔(ISI)时达到最大值,从而在200 ms的ISI时将IPSP降低至其控制幅度的80 +/- 2%。当在调节序列后2 s采样时,由20赫兹施加15个刺激的条件序列引发的IPSP增强为对照的119 +/- 1%。增强衰减的时间常数为10 s。我们测试了PPD和增强功能是否能改变IPSP防止产生动作电位的能力。由恒定振幅的去极化电流注入触发的一连串动作电位可通过刺激IPSP中断。如果此IPSP是一对IPSP中的第二个,则在阻止PPD导致的峰值方面效果不佳。相比之下,增强型IPSP在阻止峰值方面更为有效。当通过不同幅度的去极化电流注入触发动作电位时,获得了相同的结果,这种操作在每次试验之间产生几乎相同的尖峰时间,并且近似于这些神经元的体内行为。这些结果表明,抑制的短期可塑性可以改变纹状体的输出,因此可能是涉及纹状体的行为过程中信息处理的重要组成部分。

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