Morphine augments excitatory synaptic transmission in the dentate gyrus through GABAergic disinhibition
Morphine augments excitatory synaptic transmission in the dentate gyrus through GABAergic disinhibition
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DOI：
10.1016/s0168-0102(00)00177-2
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发表时间：
2000-12-01
影响因子：
2.9
通讯作者：
Ikegaya, Y
中科院分区：
文献类型：
--
作者：
Akaishi, T;Saito, H;Ikegaya, Y
本研究使用大鼠海马切片制剂研究吗啡对齿状回突触传递和长时程增强 (LTP) 的影响。分别从齿状分子层和颗粒层记录由刺激穿通路径引起的场兴奋性突触后电位（fEPSP）和群体尖峰（PS）。使用 10 μM 吗啡后，PS 幅度在 10 分钟内逐渐增加，最终增强约 50%。该现象呈浓度依赖性，并被μ阿片受体拮抗剂纳洛酮完全消除。此外，在去抑制的海马切片中没有检测到吗啡诱导的 PS 增强，这表明吗啡的促进作用需要对齿状颗粒细胞的抑制输入。使用吗啡后，fEPSP 和破伤风诱导的 PS LTP 均未改变。这些数据支持这样的假设：μ阿片受体活性调节齿状回的抑制性循环回路，从而间接对海马兴奋性神经传递发挥调节作用。 (C) 2000 Elsevier Science Ireland Ltd 和日本神经科学学会。版权所有。
The present study investigated the effect of morphine on synaptic transmission and long-term potentiation (LTP) in the dentate gyrus using rat hippocampal slice preparations. Field excitatory postsynaptic potential (fEPSP) and population spike (PS), evoked by stimulation of the perforant path, were recorded from the dentate molecular layer and the stratum granulosum, respectively. Following application of 10 muM morphine, PS amplitude increased gradually in 10 min and was eventually potentiated by approximate to 50%. The phenomenon showed a concentration-dependent manner and was completely canceled by naloxone, a mu opioid receptor antagonist. Furthermore, morphine-induced PS augmentation was not detected in disinhibited hippocampal slices, which suggests that the inhibitory input to the dentate granule cells was required for the facilitatory effect of morphine. Neither fEPSP nor tetanus-induced LTP of PS was altered by morphine application. The data support the hypothesis that mu opioid receptor activity modulates inhibitory recurrent circuits in the dentate gyrus and thereby, indirectly plays a regulatory role for hippocampal excitatory neurotransmission. (C) 2000 Elsevier Science Ireland Ltd and the Japan Neuroscience Society. All rights reserved.