Excitatory stimulation during postsynaptic inhibition induces long-term depression in hippocampus in vivo.
Excitatory stimulation during postsynaptic inhibition induces long-term depression in hippocampus in vivo.
复制标题
突触后抑制过程中的兴奋性刺激会引起体内海马体的长期抑制。
DOI：
10.1152/jn.1994.72.6.3009
复制
发表时间：
1994
影响因子：
2.5
通讯作者：
Berger,TW
中科院分区：
文献类型：
--
作者：
Thiels,E;Barrionuevo,G;Berger,TW
1.作为努力的一部分，以评估理论推导的原则突触修饰的生物学可接受性，我们研究了活动依赖性的长期抑郁症（LTD）的麻醉成年大鼠海马中的多巴胺能传递。单脉冲刺激（0.1Hz）连合传入纤维诱发的CA 1锥体细胞场电位在配对脉冲刺激（0.5Hz）同一通路前后记录。当成对的刺激间隔（ISI）较短（25 ms）时，150或200对脉冲的序列产生了对CA 1锥体神经元的连合输入的鲁棒LTD，但当ISI较长（1，000 ms）时则没有。2.配对脉冲刺激与短，但不与长ISI也与显着抑制锥体细胞发射后的第二个脉冲对，尽管事实上，兴奋性输入促进与短ISI范式。锥体细胞活性的抑制介导的输入的锥体细胞从本地γ-氨基丁酸（GABA）释放interneurons激活连合纤维和/或CA 1经常性侧支，因为抑制消除了本地管理的选择性GABAA受体拮抗剂，荷包牡丹碱（50 μ M），附近的记录网站。3. GABA能中间神经元的突触后输入对于LTD的诱导是必要的，因为在荷包牡丹碱存在下，短ISI配对脉冲刺激不能产生LTD。4. N-甲基-D-天冬氨酸（NMDA）受体介导的兴奋也是诱导LTD所必需的，因为在记录部位附近给予选择性NMDA受体拮抗剂D-2-氨基-5-膦戊酸（100 μ M）可阻止LTD的发展。（250字处删节）
1. As part of an effort to evaluate the biological plausibility of theoretically derived principles of synaptic modification, we studied activity-dependent long-term depression (LTD) of glutamatergic transmission in the hippocampus of anesthetized adult rats. Field potentials of CA1 pyramidal cells evoked by single-pulse stimulation (0.1 Hz) of the commissural afferents were recorded before and after paired-pulse stimulation (0.5 Hz) of the same pathway. A train of 150 or 200 paired pulses produced robust LTD of the commissural input to the CA1 pyramidal neurons when the interstimulus interval (ISI) of the pairs was short (25 ms) but not when the ISI was long (1,000 ms). 2. Paired-pulse stimulation with the short but not with the long ISI also was associated with pronounced inhibition of pyramidal cell firing upon the second pulse of a pair, despite the fact that the excitatory input was facilitated with the short-ISI paradigm. The inhibition of pyramidal cell activity was mediated by input to the pyramidal cells from local gamma-aminobutyric acid (GABA)-releasing interneurons activated by commissural fibers and/or CA1 recurrent collaterals, because the inhibition was eliminated by local administration of the selective GABAA receptor antagonist, bicuculline (50 microM), near the recording site. 3. Postsynaptic input from GABAergic interneurons was necessary for the induction of LTD, because short-ISI paired-pulse stimulation failed to produce LTD in the presence of bicuculline. 4. N-methyl-D-aspartate (NMDA) receptor-mediated excitation also was necessary for the induction of LTD, because administration of the selective NMDA receptor antagonist, D-2-amino-5-phosphonvaleric acid (100 microM), near the recording site prevented the development of LTD.(ABSTRACT TRUNCATED AT 250 WORDS)