Fig. 5
A schematic diagram of the synthesis and transport of GABA signaling affected by FPN in this study. (1) GABA is produced enzymatically through the activity of glutamate decarboxylase (GAD 65/67). The FPN exposure significantly decreased the mRNA levels of GAD 67, which might reduce GABA synthesis. (2) GABA transporters (GAT) facilitate the transportation of GABA through the cellular space. The deficiency of GAT1 would affect the function of GABA transportation and might be associated with IL-2 and IFN-γ increase by FPN exposure. (3) Activation of GABAA receptors occurs upon GABA binding, leading to either the efflux or influx of Cl−. After FPN treatment, the mRNA expression of subunits of β2 and δ were notably increased which might be a compensatory mechanism to overcome the adverse effects of FPN-induced dysregulation of GABAergic genes. Parts of the figure were drawn by using pictures from Servier Medical Art. Servier Medical Art by Servier is licensed under a Creative Commons Attribution 3.0 Unported License (https://creativecommons.org/licenses/by/3.0/)