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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Synaptic kainate receptors in CA1 interneurons gate the threshold of theta-frequency-induced long-term potentiation
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Synaptic kainate receptors in CA1 interneurons gate the threshold of theta-frequency-induced long-term potentiation

机译:CA1中间神经元中的突触海藻酸盐受体门控theta频率诱导的长期增强的阈值。

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摘要

Theta oscillations (4-12 Hz) in neuronal networks are known to predispose the synapses involved to plastic changes and may underlie their association with learning behaviors. The lowered threshold for synaptic plasticity during theta oscillations is thought to be due to decreased GABAergic inhibition. Interneuronal kainate receptors (KARs) regulate GABAergic transmission and are implicated in theta activity; however, the physiological significance of this regulation is unknown. In rat hippocampus, we show that during theta activity, there is excitatory postsynaptic drive to CA1 interneurons mediated by KARs. This promotes feedforward inhibition of pyramidal neurons, raising the threshold for induction of theta-burst long-term potentiation. These results identify a novel mechanism whereby the activation of postsynapticKARsinCA1interneurons gate changes in synaptic efficacy to a physiologically relevant patterned stimulation.
机译:已知神经元网络中的Theta振动(4-12 Hz)易诱发涉及塑性变化的突触,并可能将其与学习行为联系起来。在θ振荡期间突触可塑性的阈值降低被认为是由于降低的GABA能抑制。神经内海藻酸酯受体(KARs)调节GABA能传递,并参与θ活性。但是,这种调节的生理意义尚不清楚。在大鼠海马中,我们显示在theta活动期间,存在由KAR介导的CA1间神经元兴奋性突触后驱动。这促进了锥体神经元的前馈抑制,从而提高了诱导theta-burst长期增强的阈值。这些结果确定了一种新的机制,据此,突触后KARsinCA1interneurons门的激活改变了突触效力对生理学相关的模式刺激。

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