Long-Lasting GABA-Mediated Depolarization Evoked by High-Frequency Stimulation in Pyramidal Neurons of Rat Hippocampal Slice Is Attributable to a Network-Driven, Bicarbonate-Dependent K+ Transient
Long-Lasting GABA-Mediated Depolarization Evoked by High-Frequency Stimulation in Pyramidal Neurons of Rat Hippocampal Slice Is Attributable to a Network-Driven, Bicarbonate-Dependent K+ Transient
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大鼠海马切片锥体神经元高频刺激引起的持久 GABA 介导的去极化可归因于网络驱动、碳酸氢盐依赖性 K 瞬变
DOI：
10.1523/jneurosci.17-20-07662.1997
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
J. Voipio
中科院分区：
文献类型：
--
作者：
K. Kaila;K. Lamsa;S. Smirnov;T. Taira;J. Voipio
在离子型谷氨酸受体拮抗剂存在下，高频刺激（HFS）可在大鼠海马脑片CA 1区锥体神经元诱发双相GABA A介导的突触后反应。在本实验中，使用尖微电极、全细胞技术和K+选择性微电极，在靠近记录部位的辐射层中施加HFS序列（100 Hz 40个脉冲）诱发短暂的超极化IPSP（hIPSP），其转变为延长的（2-3秒）去极化（GABA介导的去极化突触后电位; GDPSP）。突触后电流（hIPSC和GDPSC）的I-V关系具有明显的特征：hIPSC和早期GDPSC表现出外向整流，而晚期GDPSC随着正电压阶跃降低至零或以上（内向整流），但通常没有明显的逆转。两种不同的电流有助于GDPSP的产生，这一点也从以下发现中得到了证明：在峰值或晚期GDPSP的第二个HFS串诱导了迅速的GABAA介导的超极化。GDPSP/C依赖于碳酸氢盐的可用性，但不依赖于间质或锥体内碳酸酐酶活性。HFS列车引起了快速GABAA介导的碳酸氢盐依赖性增加细胞外K+浓度（[K+]o），和GDPSP后，K+瞬态亚能斯特的方式。[K+]o位移的空间和药理学特征表明，它是由GABA能中间神经元的局部网络产生的。GDPSP的短暂上升阶段与细胞内Cl−的K+依赖性积累有关。此后，一种非突触机制，[K+] o漂移的直接去极化效应，负责GDPSP最显著的特征：其大幅度和延长的持续时间。
Biphasic GABAA-mediated postsynaptic responses can be readily evoked in CA1 pyramidal neurons of rat hippocampal slices by high-frequency stimulus (HFS) trains in the presence of ionotropic glutamate receptor antagonists. In the present experiments with sharp microelectrodes, whole-cell techniques, and K+-selective microelectrodes, an HFS train (40 pulses at 100 Hz) applied in stratum radiatum close to the recording site evoked a brief hyperpolarizing IPSP (hIPSP), which turned into a prolonged (2–3 sec) depolarization ( GABA-mediated depolarizing postsynaptic potential; GDPSP). The I–V relationships of the postsynaptic currents (hIPSC and GDPSC) had distinct characteristics: the hIPSC and the early GDPSC showed outward rectification, whereas the late GDPSC was reduced with positive voltage steps to zero or beyond (inward rectification), but often no clear reversal was seen. That two distinct currents contribute to the generation of the GDPSP was also evident from the finding that a second HFS train at peak or late GDPSP induced a prompt GABAA-mediated hyperpolarization. The GDPSP/C was dependent on the availability of bicarbonate, but not on interstitial or intrapyramidal carbonic anhydrase activity. The HFS train evoked a rapid GABAA-mediated bicarbonate-dependent increase in the extracellular K+ concentration ([K+]o), and the GDPSP followed the K+ transient in a sub-Nernstian manner. The spatial and pharmacological characteristics of the [K+]o shift indicated that it is generated by a local network of GABAergic interneurons. The brief ascending phase of the GDPSP is linked to a K+-dependent accumulation of intracellular Cl−. Thereafter, a nonsynaptic mechanism, a direct depolarizing effect of the [K+]oshift, is responsible for the most conspicuous characteristics of the GDPSP: its large amplitude and prolonged duration.
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