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. Author manuscript; available in PMC: 2016 Jan 31.

Published in final edited form as: J Neurochem. 2014 Sep 18;132(3):354–366. doi: 10.1111/jnc.12936

Fig. 1 — a, Stylized traces ( ) depict time-dependent, biphasic changes in NMDA-evoked increases in [Ca²⁺]_i following exposure to HIV-1 Tat for the time indicated above the trace. The previously reported (Krogh et al. 2014) sequence of events listed below the traces indicates that Tat activation of an LRP/Src kinase pathway resulted in NMDAR potentiation. Subsequently, NMDARs adapted following activation of the NOS/sGC/PKG signaling pathway. Identifying downstream effector(s) of PKG is the goal of this study. b, Representative pseudocolor images (scale bar = 100 μm) show peak response to NMDA (10μM, 30 s) in primary hippocampal neurons treated with Tat for the time indicated in the image panel. Images were scaled from 0 to 700 nM as indicated by the color bar on the y-axis.

Inline graphic — a, Stylized traces ( ) depict time-dependent, biphasic changes in NMDA-evoked increases in [Ca²⁺]_i following exposure to HIV-1 Tat for the time indicated above the trace. The previously reported (Krogh et al. 2014) sequence of events listed below the traces indicates that Tat activation of an LRP/Src kinase pathway resulted in NMDAR potentiation. Subsequently, NMDARs adapted following activation of the NOS/sGC/PKG signaling pathway. Identifying downstream effector(s) of PKG is the goal of this study. b, Representative pseudocolor images (scale bar = 100 μm) show peak response to NMDA (10μM, 30 s) in primary hippocampal neurons treated with Tat for the time indicated in the image panel. Images were scaled from 0 to 700 nM as indicated by the color bar on the y-axis.