LONG-TERM POTENTIATION INVOLVES ENHANCED SYNAPTIC EXCITATION RELATIVE TO SYNAPTIC INHIBITION IN GUINEA-PIG HIPPOCAMPUS
LONG-TERM POTENTIATION INVOLVES ENHANCED SYNAPTIC EXCITATION RELATIVE TO SYNAPTIC INHIBITION IN GUINEA-PIG HIPPOCAMPUS
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DOI：
10.1113/jphysiol.1987.sp016875
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发表时间：
1987-12-01
影响因子：
5.5
通讯作者：
WIGSTROM, H
中科院分区：
文献类型：
--
作者：
ABRAHAM, WC;GUSTAFSSON, B;WIGSTROM, H
1.在CA 1区辐射层中行进的海马锥体细胞传入的Tetanization诱导长时程增强（l. t. p.）的细胞外记录的兴奋性突触后电位（ep. s. p. s），并增加了细胞放电的数量，如通过细胞外群体尖峰测量的，对于给定大小的场ep. p. s. p.。在豚鼠海马脑片制备中研究了E-S增强。2.通过对一系列刺激强度的测量，构建了强直刺激前后E-S关系图。辐射层中传入神经的Tetanization使峰电位阈值降低24%，而γ-氨基丁酸拮抗剂印防己毒素（PTX）使放电阈值降低72%。PTX和破伤风的顺序管理，以任何顺序，导致没有更多的变化，在E-S阈值比单独应用PTX。3.细胞外突触电位，匹配的初始斜率之前和之后，通过调整刺激强度，表现出增加的峰值振幅和增加的峰值潜伏期后强直。PTX产生类似但更大的百分比变化。然而，PTX存在下的Tetanization并没有改变场电位波形。4.细胞内突触后电位（p. s. p. s）也匹配的初始斜率之前和之后强直。Tetanization诱导的p. s. p.形状变化类似于细胞外观察到的变化，即在较少抑制的方向上。这些变化在PTX的存在下没有发生。5.在去极化锥体细胞中，使用填充QX-314的微电极研究抑制性p. s. p. s（i. p. s. p. s）。辐射层传入神经的破伤风化使19个细胞中的8个产生ip增加。这些增加通常归因于复发性抑制途径中的活性增加。肺泡的破伤风化未能产生任何持续的ipsp振幅增加。6.辐射层传入神经的Tetanization降低了细胞内ipsp与场epsp的比值，低于群体峰电位阈值的刺激强度。在种群高峰阈值以上，该比值趋于破伤风前水平。7.结果表明，E-S增强是由于给定初始斜率的突触电位所达到的去极化水平增加所致。这些发现支持这一假设，即强直诱导更大的l. t. p.兴奋性输入到锥体细胞比输入到前馈抑制性中间神经元。
1. Tetanization of hippocampal pyramidal cell afferents travelling in stratum radiatum of area CA1 induces both long-term potentiation (l.t.p.) of extracellularly recorded excitatory postsynaptic potentials (e.p.s.p.s), and an increase in the number of cells firing, as measured by the extracellular population spike, for a given sized field e.p.s.p. The mechanism of this latter change, known as e.p.s.p.-spike (E-S) potentiation, was investigated in the guinea-pig hippocampal slice preparation. 2. Plots of the E-S relation before and afater tetanization were constructed from measures taken over a series of stimulus strengths. Tetanization of afferents in stratum radiatum decreased the spike threshold by 24%, while the .gamma.-aminobutyric acid antagonist picrotoxin (PTX) decreased spike threshold by 72%. Sequential administration of PTX and tetanization, in either order, resulted in no more change in the E-S threshold than did PTX application alone. 3. Extracellular synaptic potentials, matched for initial slope before and after tetanization by adjusting the stimulus strength, showed an increased peak amplitude and increased peak latency following tetanization. PTX produced similar but larger percentage changes. Tetanization in the presence of PTX, however, did not alter the field potential wave shape. 4. Intracellular postsynaptic potentials (p.s.p.s) were also matched for initial slope before and after tetanization. Tetanization induced p.s.p. shape changes similar to those observed extracellularly, i.e. in the direction of less inhibition. Such changes did not occur in the presence of PTX. 5. Inhibitory p.s.p.s (i.p.s.p.s) were studied in depolarized pyramidal cells with microelectrodes filled with QX-314. Tetanization of afferents in stratum radiatum produced i.p.s.p. increases in eight of nineteen cells. These increases were generally attributable to an increased activity in the recurrent inhibitory pathway. Tetanization of the alveus failed to produce any lasting increases in the i.p.s.p. amplitude. 6. Tetanization of afferents in stratum radiatum decreased the ratio of the intracellular i.p.s.p. to field e.p.s.p. over stimulus strengths below population spike threshold. Above population spike threshold, the ratio tended towards its pretetanization level. 7. The results indicate that E-S potentiation results from an increase in the level of depolarization reached by a synaptic potential of given initial slope. These findings support the hypothesis that tetanization induces greater l.t.p. of excitatory inputs onto pyramidal cells than of inputs onto feed-forward inhibitory interneurones.