Leung L Stan, Peloquin Pascal, Canning Kevin J
Department of Physiology and Pharmacology, University of Western Ontario, London, Ontario, Canada.
Hippocampus. 2008;18(10):1008-20. doi: 10.1002/hipo.20458.
Paired-pulse depression (PPD), a short-term neural plasticity, was studied in hippocampal CA1 of urethane-anesthetized rats in vivo, using field potential recordings and current source density analysis. PPD was robust when an ipsilateral CA3 (iCA3) conditioning pulse of moderate stimulus intensity was followed 30-200 ms later by a contralateral CA3 (cCA3) test pulse; the ratio of the conditioned (C) to the nonconditioned (NC) response, as measured by the peak excitatory sink at the apical dendrites, ranged from 0.6 to 0.8. An alveus conditioning pulse evoked a large antidromic population spike in CA1 and a modest depression of the CA3-evoked excitatory sink (C/NC ratio of approximately 0.85). High-intensity paired pulses, both delivered to iCA3, also showed PPD of the proximal excitatory sinks; however, paired-pulse facilitation of the dendritic sinks was found at the mid-apical dendrites, >250 microm from the soma. Local injection of GABA(A) antagonist picrotoxin or bicuculline increased the C/NC ratio at IPIs of <150 ms, as well as the ratio of the amplitude of the population spikes (P2/P1; where P2 and P1 are the population spikes evoked by the second and first pulse, respectively). GABA(B) receptor antagonists, CGP35348 given intracerebroventricularly or CGP56999A administered locally, increased C/NC and P2/P1 at IPIs of 150-400 ms. It is concluded that conditioned depression of the excitatory sinks was caused by mainly feedforward and some feedback inhibition at the apical dendrites. GABA(A)-mediated postsynaptic inhibition dominated at early latencies, while GABA(B)-mediated inhibition prevailed at long latencies, probably at both presynaptic and postsynaptic sites. PPD of the excitatory sinks provides a measure of population dendritic inhibition in vivo.
双脉冲抑制（PPD）是一种短期神经可塑性，本研究在体内对氨基甲酸乙酯麻醉大鼠的海马CA1区进行，采用场电位记录和电流源密度分析。当同侧CA3（iCA3）中等刺激强度的条件刺激脉冲在30 - 200毫秒后跟随对侧CA3（cCA3）测试脉冲时，PPD很明显；通过顶端树突处的兴奋性电流池峰值测量的条件（C）与非条件（NC）反应的比率在0.6至0.8之间。海马槽条件刺激脉冲在CA1区诱发一个大的逆向群体峰电位，并使CA3诱发的兴奋性电流池适度抑制（C/NC比率约为0.85）。高强度双脉冲，均施加于iCA3，也显示近端兴奋性电流池的PPD；然而，在距胞体>250微米的顶端树突中部发现树突电流池的双脉冲易化。局部注射GABA(A)拮抗剂印防己毒素或荷包牡丹碱可增加<150毫秒的脉冲间隔时的C/NC比率，以及群体峰电位的幅度比率（P2/P1；其中P2和P1分别是由第二个和第一个脉冲诱发的群体峰电位）。GABA(B)受体拮抗剂，脑室内注射CGP35348或局部施用CGP56999A，可增加150 - 400毫秒的脉冲间隔时的C/NC和P2/P1。结论是，兴奋性电流池的条件抑制主要由顶端树突处的前馈和一些反馈抑制引起。GABA(A)介导的突触后抑制在早期潜伏期占主导，而GABA(B)介导的抑制在长潜伏期占优势，可能在突触前和突触后部位均如此。兴奋性电流池的PPD提供了体内群体树突抑制的一种测量方法。
