Figure 1
From: GSK-3β deletion in dentate gyrus excitatory neuron impairs synaptic plasticity and memory
Expression of Cre recombinase selectively deletes GSK-3β in DG excitatory neurons of GSK-3β loxp mice. (a) Schematic representation of pAAV-CaMKII-Cre-2A-eGFP and the empty pAAV-CaMKII-eGFP vector. (b) A representative image showing efficient virus infection in DG and the mossy fibers. (c,d) Injection of Cre recombinase into hippocampal DG of GSK-3β loxp mice for 1-m efficiently downregulated GSK-3β protein level measured by Western blotting (n = 3 each group). (e) The reduced GSK-3β activity in DG extracts after Cre recombinase injection (n = 3 each group). (f) Deletion of GSK-3β in DG neurons by Cre recombinase injection measured by immunohistochemistry, scale bars, 100 μm. (g,h) Specific deletion of GSK-3β in DG excitatory neurons measured by co-immunofluorescence of GFP with CaMKII but not with GAD67 antibody, scale bars, 10 μm. (i,j) Deletion of GSK-3β did not significantly affect GSK-3α in DG subset (n = 3 each group). Data were presented as mean ± s.e.m. unpaired t test, **P < 0.01, ***P < 0.001 versus Vector. The absence of asterix indicates that the difference is not significant.
