Neuroscience Center, University of Helsinki, 00014 Helsinki, Finland.
J Neurosci. 2012 Dec 12;32(50):18215-26. doi: 10.1523/JNEUROSCI.2327-12.2012.
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 postsynaptic KARs in CA1 interneurons gate changes in synaptic efficacy to a physiologically relevant patterned stimulation.
神经元网络中的θ振荡（4-12 Hz）已知会使涉及的突触易于发生塑性变化，并可能是其与学习行为相关联的基础。在θ振荡期间，突触可塑性的阈值降低被认为是由于 GABA 能抑制的减少。中间神经元的海人藻酸受体（KAR）调节 GABA 能传递，并且与θ活动有关；然而，这种调节的生理意义尚不清楚。在大鼠海马体中，我们表明在θ活动期间，KAR 介导了 CA1 中间神经元的兴奋性突触驱动。这促进了对锥体神经元的前馈抑制，提高了诱导θ爆发长时程增强的阈值。这些结果确定了一种新的机制，即 CA1 中间神经元中突触后 KAR 的激活可以控制突触效能的变化，使其适应生理相关的模式刺激。
