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. 2016 Apr 18;12:1744806916644927. doi: 10.1177/1744806916644927

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© The Author(s) 2016

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 3.0 License (http://www.creativecommons.org/licenses/by-nc/3.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page(https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 4. — The JAK inhibitor tofacitinib had no effect on IFNγ-induced NMDA currents. (a) Tofacitinib (1 mM) addition to the pipette solution did not affect the IFNγ-induced NMDA current. In this experimental system, the control corresponds to the IFNγ-induced NMDA currents recorded immediately after patch clamping. (b) Bar graphs show the average rate of NMDA current enhancement by IFNγ at the start of patch-clamp recording and 30 min later. The peak amplitude of the IFNγ-induced NMDA currents did not change compared with the control recording. This confirmed that IFNγ enhances neuronal NMDA-induced inward current via the microglial IFNγ receptor. IFNγ: interferon-gamma; NMDA: N-methyl-d-aspartate; n.s.: not significant.