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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 6. — The enhancement of NMDA-induced inward current by IFNγ was mediated by CCR2. (a) Bath application of the CCR2 antagonist Teijin compound 1 hydrochloride (10 μM, 5.5 min) blocked the IFNγ-induced enhancement of NMDA currents. (b) The peak amplitude of the NMDA-induced currents after simultaneous application of Teijin compound 1 hydrochloride and IFNγ was 95.0 ± 5.3% that of baseline. IFNγ likely increases the NMDA-induced inward current in SG neurons via CCR2. IFNγ: interferon-gamma; NMDA: N-methyl-d-aspartate; n.s.: not significant.