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 [
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Figure 1Characterization of spontaneously epileptic mice 3 weeks after intraamygdaloid injection of KA. (
A–
D) Representative cresyl violet–stained coronal brain section showing the hippocampal formation contralateral (
A and
C) or ipsilateral (
B and
D) to the KA injection. Note the CA3 selective cell loss in the ipsilateral hippocampus (
B and
D). (
E and
F) Adjacent coronal brain section from the same animal stained with the nuclear stain DAPI showing an increase in the number of cell nuclei in the injured CA3. (
G and
H) The same section stained with NFM indicating the presence of dense neuronal networks within the injured CA3. (
I–
N) ADK immunoreactivity within the hippocampal formation visualized with diaminobenzidine contralateral (
I,
K, and
M) or ipsilateral (
J,
L, and
N) to the KA injection. Note the focal overexpression of ADK in the ipsilateral CA3.
I–
L are from the same animal and adjacent to those shown in
A–
H.
M and
N are derived from the same animal at a more caudal location, representing the level of cell transplantations (see Figure
10). Arrows in
J and
N point to upregulated ADK in ipsilateral CA3. (
O–
R) Confocal analysis of ADK (red) and GFAP (green) immunoreactivity in the contralateral (
O and
P) and ipsilateral (
Q and
R) CA3. Note prominent astrogliosis (GFAP) and overexpression and redistribution of ADK in the ipsilateral CA3 (
Q and
R). Bottom: Representative EEG recordings obtained from electrodes inserted into the ipsilateral CA3 or CA1 or placed onto the cortex. Scale bars: 300 μm (
A,
B,
I,
J,
M, and
N), 75 μm (
C and
D), 37.5 μm (
E,
F,
G,
H,
K, and
L), 12 μm (
O and
Q), and 5 μm (
P and
R). EEG scale bar: 2 s.
