Paired stimulation between CA3 and CA1 alters excitability of CA3 in the rat hippocampus.

Paired stimulation between CA3 and CA1 alters excitability of CA3 in the rat hippocampus.
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CA3 和 CA1 之间的配对刺激会改变大鼠海马 CA3 的兴奋性。

DOI:
10.1016/j.neulet.2012.11.058
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发表时间:
2013
影响因子:
2.5
通讯作者:
Nishida Y
Nishida Y
中科院分区:
医学4区
文献类型:
--
作者:
Ohta H;Sakai S;Ito S;Ishizuka T;Fukazawa y Kemuriyama T;Tandai-Hiruma M;Mushiake H;Sato Y;Yawo H;Nishida Y

文献摘要

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人们普遍认为可塑性的程度局限于突触和突触后细胞内信号级联周围的区域。我们研究了与突触前神经元 (CA3) 兴奋性相关并受突触后神经元 (CA1) 放电调节的长程逆行可塑性的存在。我们使用在 CA1 和 CA3 神经元中表达通道视紫红质 2 (ChR2) 的转基因大鼠的急性海马切片。我们采用了并行光刺激技术,该技术能够在 CA3 或 CA1 神经元中稳健且独立地激发动作电位。光学诱发 CA3 放电与 CA1 同时放电或长时间刺激后 CA1 抑制配对。通过测量光诱发放电率(Opt-FR)来监测突触前兴奋性。我们发现CA3神经元的Opt-FR由于同步突触前和突触后配对刺激而长期上调,但在突触后抑制期间因突触前刺激而下调。 NMDA 受体阻断或秋水仙碱预孵育均延迟了配对依赖性上调和下调。这一发现表明 CA3 兴奋性受 CA3 放电时 CA1 神经元活动的调节。
It is generally accepted that the extent of plasticity is localized to the region around synapses and post-synaptic intracellular signaling cascades. We investigated the presence of long-range retrograde plasticity associated with excitability at pre-synaptic neurons (CA3) and regulated by the firing of post-synaptic neurons (CA1). We used acute hippocampus slices from transgenic rats expressing channelrhodopsin-2 (ChR2) in both CA1 and CA3 neurons. We employed a parallel photostimulation technique, which enabled robust and independent evocation of action potentials in either CA3 or CA1 neurons. Optically evoked CA3 firings were paired either with CA1 simultaneous firings or with CA1 suppression after the prolonged stimulation. Pre-synaptic excitability was monitored by measuring the optically-evoked firing rate (Opt-FR). We found that the Opt-FR of CA3 neurons was long-term up-regulated as a result of synchronous pre- and post-synaptic pairing stimulation, but down-regulated by the pre-synaptic stimulation during post-synaptic suppression. Both pairing-dependent up-regulation and down-regulation were retarded by NMDA receptor blocking or colchicine preincubation. This finding suggest that CA3 excitability is regulated by CA1 neuron activity at the time of CA3 firing.