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首页> 外文期刊>The European Journal of Neuroscience >Synaptic activation of GABA(B) receptors regulates neuronal network activity and entrainment.
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Synaptic activation of GABA(B) receptors regulates neuronal network activity and entrainment.

机译：GABA（B）受体的突触激活调节神经元网络活动和夹带。

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In the mammalian central nervous system, GABA(B) receptors mediate slow pre- and postsynaptic inhibition. Using rat hippocampal slices we investigated the role of synaptic GABA(B) receptors in regulating kainate-induced subthreshold neuronal network oscillations in the gamma frequency range (25-80 Hz). The GABA(B) receptor agonist baclofen largely eliminated gamma oscillations. The GABA(B) receptor antagonist CGP55845 reversed this action of baclofen but alone did not alter the power or frequency of ongoing oscillations. To examine the role of synaptically released GABA on network activity, we electrically stimulated stratum radiatum of CA3 whilst recording gamma oscillations from stratum pyramidale. Single stimuli produced a pronounced transient (up to 1 s in duration) inhibition of gamma frequency oscillations. This stimulus-induced shutdown of network activity was enhanced by the GABA uptake inhibitor tiagabine and largely inhibited by CGP55845. Multiple stimuli delivered at frequencies of 1-3 Hz resulted in an activity-dependent fatigue of the inhibition of gamma activity, such that, after a number of stimuli, oscillations could be detected tens of milliseconds after the stimulus. Interestingly, this activity-dependent fatigue of inhibition uncovered a stimulus-dependent temporal entrainment of the gamma oscillations. Furthermore, the amount of repetitive synaptic input that was required to cause this entrainment was dramatically reduced by GABA(B) receptor antagonism such that it was evident within just a few stimuli. These data suggest that convergent afferent synaptic activity can alter the precise temporal arrangement of neuronal network activity. Furthermore, the flow of such information into a functioning neuronal network is highly regulated by GABA(B) receptor-mediated synaptic inhibition.
机译：在哺乳动物的中枢神经系统中，GABA（B）受体介导缓慢的突触前和突触后抑制。使用大鼠海马切片，我们研究了突触的GABA（B）受体在伽马频率范围（25-80 Hz）中调节海藻酸盐诱导的亚阈下神经元网络振荡的作用。 GABA（B）受体激动剂巴氯芬在很大程度上消除了伽马振荡。 GABA（B）受体拮抗剂CGP55845逆转了巴氯芬的这一作用，但单独使用并没有改变正在进行的振荡的能力或频率。为了检查突触释放的GABA在网络活动中的作用，我们用电刺激了CA3的辐射层，同时记录了锥体层的伽马振荡。单个刺激产生了明显的瞬变（持续时间长达1 s），抑制了伽马频率振荡。这种刺激诱导的网络活动关闭被GABA摄取抑制剂替加宾碱增强，并在很大程度上被CGP55845抑制。以1-3 Hz的频率传递的多个刺激导致伽玛活性抑制的活动依赖性疲劳，这样，在多次刺激之后，可以在刺激后数十毫秒内检测到振荡。有趣的是，这种与活动有关的抑制疲劳揭示了伽马振荡的与刺激有关的时间夹带。此外，GABA（B）受体拮抗作用极大地减少了引起这种夹带的重复性突触输入量，因此仅在少数刺激中就很明显。这些数据表明会聚的突触活动可以改变神经元网络活动的精确的时间安排。此外，此类信息流入功能性神经元网络的过程受到GABA（B）受体介导的突触抑制的高度调节。

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