In the somatosensory cortex, inhibitory networks are involved in low frequency sensory input adaptation/habituation that can be observed as a paired-pulse depression when using a dual stimulus electrophysiological paradigm. Given that astrocytes have been shown to regulate inhibitory interneuron activity, we hypothesized that astrocytes are involved in cortical sensory adaptation/habituation and constitute effectors of the 5HT-mediated increase in frequency transmission. Using extracellular recordings of evoked excitatory postsynaptic potentials (eEPSPs) in layer II/III of somatosensory cortex, we used various pharmacological approaches to assess the recruitment of astrocyte signaling in paired-pulse depression and serotonin-mediated increase in the paired-pulse ratio (pulse 2/pulse 1). In the absence of neuromodulators or pharmacological agents, the first eEPSP is much larger in amplitude than the second due to the recruitment of long-lasting evoked GABA_A-dependent inhibitory activity from the first stimulus. Disruption of glycolysis or mGluR5 signaling resulted in a very similar loss of paired-pulse depression in field recordings. Interestingly, paired-pulse depression was similarly sensitive to disruption by ATP P2Y and adenosine A2A receptor antagonists. In addition, we show that pharmacological disruption of paired-pulse depression by mGluR5, P2Y, and glycolysis inhibition precluded serotonin effects on frequency transmission (typically increased the paired-pulse ratio). These data highlight the possibility for astrocyte involvement in cortical inhibitory activity seen in this simple cortical network and that serotonin may act on astrocytes to exert some aspects of its modulatory influence.

在体感皮层中，抑制网络参与了低频感官输入的适应性/适应性，当使用双重刺激电生理范式时，可以将其视为成对的脉冲压抑。考虑到星形胶质细胞已显示出调节抑制性中枢神经元活性，我们假设星形胶质细胞参与皮层感觉适应/适应，并构成5HT介导的频率传递增加的效应器。使用体感皮质的II / III层中诱发的兴奋性突触后突触电位（eEPSPs）的细胞外记录，我们使用了多种药理学方法评估了成对脉冲抑制中星形胶质细胞信号的募集和5-羟色胺介导的成对脉冲比率（脉冲）的增加。 2 /脉冲1）。在没有神经调节剂或药理剂的情况下，_甲从第一刺激依赖性抑制活性。糖酵解或mGluR5信号的破坏导致现场记录中成对脉冲抑制的损失非常相似。有趣的是，成对脉冲抑制对ATP P2Y和腺苷A2A受体拮抗剂的破坏同样敏感。此外，我们显示，通过mGluR5，P2Y和糖酵解抑制作用的成对脉冲抑制的药理学破坏阻止了血清素对频率传递的影响（通常增加了成对脉冲比）。这些数据强调了星形胶质细胞参与这种简单的皮质网络所见的皮质抑制活性的可能性，并且血清素可能作用于星形胶质细胞以发挥其调节作用的某些方面。