Fitzpatrick J S, Akopian G, Walsh J P
Leonard Davis School of Gerontology and Program in Neuroscience, University of Southern California, Los Angeles, California 90089-0191, USA.
J Neurophysiol. 2001 May;85(5):2088-99. doi: 10.1152/jn.2001.85.5.2088.
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.
利用细胞内记录技术，在成年大鼠纹状体脑片中研究了抑制性突触处的两种短期可塑性形式。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微摩尔）和D,L-2-氨基-5-膦酰基戊酸（50微摩尔）存在的情况下，纹状体内刺激产生了抑制性突触后电位（IPSP），其反转电位为-76±1（标准误）毫伏，且对荷包牡丹碱（30微摩尔）敏感。IPSP在超极化膜电位时发生整流，部分原因是钾离子通道的激活。IPSP表现出两种短期可塑性形式，即双脉冲抑制（PPD）和突触增强。PPD持续数秒，在数百毫秒的刺激间隔（ISI）时最为明显，在200毫秒的ISI时，IPSP减小至其对照幅度的80±2%。由以20赫兹施加的15次刺激的条件刺激串引发的IPSP增强，在条件刺激串后2秒采样时为对照的119±1%。增强以10秒的时间常数衰减。我们测试了PPD和增强是否会改变IPSP阻止动作电位产生的能力。由恒定幅度的去极化电流注入触发的一串动作电位可被IPSP刺激中断。如果这个IPSP是一对IPSP中的第二个，由于PPD，它在阻断尖峰方面的效果较差。相比之下，增强的IPSP在阻断尖峰方面更有效。当由幅度变化的去极化电流注入触发动作电位时，也得到了相同的结果，这种操作在每次试验中产生几乎相同的尖峰时间，并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。
