Adenosine kinase is a target for the prediction and prevention of epileptogenesis in mice
J. Clin. Invest. Tianfu Li, et al. 118:571 doi:10.1172/JCI33737 [Go to this article.]

Figure 3
Photomicrographs of ADK immunoreactivity in coronal brain sections of adult mice, processed for immunoperoxidase staining under identical conditions. (A) Hippocampal formation of a WT brain showing a homogenous distribution of individual cells expressing ADK. (B) CA3 region (asterisk) of WT mouse at higher magnification showing the restriction of ADK expression to individual astrocytes (arrows). (C) Hippocampal formation of an Adk-Tg brain showing ubiquitous overexpression of transgenic ADK coupled with a loss of punctate staining of endogenous ADK in individual cells. Note the strong ADK immunoreactivity in pyramidal cell neurons. Dashed arrow, cortex; solid arrow, thalamus. (D) CA3 region of an Adk-Tg mouse at higher magnification showing overexpression of ADK in CA3 neurons (asterisk). (E) Spontaneous seizure recorded from the CA3 region of an Adk-Tg mouse. Trace represents 30 s of recording time. (F) Hippocampal formation of an fb-Adk-def brain showing reduced ADK staining in hippocampus and cortex (dashed arrow) compared with thalamus (solid arrow) and striatum of the same slice and compared with both WT and Adk-Tg hippocampus. (G) CA3 region of an fb-Adk-def mouse at higher magnification showing global reduction of ADK but individual remaining ADK-positive cells (arrows). Scale bars: 500 μm (A, C, and F), 50 μm (B, D, and G).