The cortex immediately surrounding a brain ischemic lesion, the peri-infarct cortex (PIC), harbors a large part of the potential to recover lost functions. However, our understanding of the neurophysiological conditions in which synaptic plasticity operates remains limited. Here we hypothesized that the chronic imbalance between excitation and inhibition of the PIC prevents the normalization of the gamma rhythm, a waveband of neural oscillations thought to orchestrate action potential trafficking. Probing the local field potential activity of the forelimb primary sensory cortex (S1FL) located in the PIC of male adult mice, we found a constant, deep reduction of low-gamma oscillation power (L-gamma; 30–50 Hz) precisely during the critical time window for recovery (1–3 weeks after stroke). The collapse of L-gamma power negatively correlated with behavioral progress in affected forelimb use. Mapping astrocyte reactivity and GABA-like immunoreactivity in the PIC revealed a parallel high signal, which gradually increased when approaching the lesion. Increasing tonic inhibition with local infusion of GABA or by blocking its recapture reduced L-gamma oscillation power in a magnitude similar to stroke. Conversely, the negative allosteric modulation of tonic GABA conductance using L655,708 or the gliopeptide ODN rescued the L-gamma power of the PIC. Altogether the present data point out that the chronic excess of ambient GABA in the PIC limits the generation of L-gamma oscillations in the repairing cortex and suggests that rehabilitative interventions aimed at normalizing low-gamma power within the critical period of stroke recovery could optimize the restitution of lost functions.

紧邻脑缺血病变的皮层，即梗死周围皮层 （PIC），具有恢复丢失功能的很大一部分潜力。然而，我们对突触可塑性运作的神经生理条件的理解仍然有限。在这里，我们假设 PIC 的兴奋和抑制之间的慢性不平衡阻止了 γ 节律的正常化，γ 节律是一种被认为可以协调动作电位运输的神经振荡波段。探测位于雄性成年小鼠 PIC 中的前肢初级感觉皮层 （S1FL） 的局部场电位活动，我们发现低 γ 振荡功率 （L-gamma;30-50 Hz） 恰好在恢复的关键时间窗口（中风后 1-3 周）持续、深度降低。L-γ 力量的崩溃与受影响的前肢使用的行为进展呈负相关。在 PIC 中绘制星形胶质细胞反应性和 GABA 样免疫反应性显示平行的高信号，当接近病灶时逐渐增加。通过局部输注 GABA 或通过阻断其再捕获来增加强直抑制作用，以类似于中风的幅度降低 L-γ 振荡能力。相反，使用 L655,708 或胶质肽 ODN 对强直性 GABA 电导的负变构调节挽救了 PIC 的 L-γ 能力。总而言之，目前的数据指出，PIC 中环境 GABA 的慢性过量限制了修复皮层中 L-γ 振荡的产生，并表明旨在使低 γ 功率在中风恢复的关键时期正常化的康复干预可以优化失去功能的恢复。