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. 2014 Jun 11;34(24):8186–8196. doi: 10.1523/JNEUROSCI.4267-13.2014

Figure 7.

Figure 7.

ACPD-elicited increases in BDNF protein are reduced in cuprizone-treated animals after cre recombination. Cre recombinase + GFAPcreERT2-floxBDNF-ROSA26 mice and Cre recombinasefloxBDNF-ROSA26 controls were injected with tamoxifen and fed cuprizone-laden food for 4 weeks before they received a single stereotaxic injection of either ACPD or saline vehicle. a, Western blots demonstrate BDNF protein in the corpus callosum of these animals. GAPDH is shown as a loading control. b, Graph represents a densitometric analysis of a Western blot of mature BDNF normalized to GAPDH and presented as percentage Cre− saline-injected control. c, Cre recombination results in a decrease in elevations of ACPD-elicited BDNF. Immunohistochemical analysis demonstrates that BDNF is eliminated from ACPD-treated GFAP+ astrocytes in the corpus callosum of cuprizone-treated Cre+ GFAPcreERT2-floxBDNF-ROSA26 mice. Western blot data were analyzed by ANOVA; *significantly different from saline-injected, cre− controls at p < 0.01; ***significantly different at p < 0.01. Each Western blot lane is from the corpus callosum of a single mouse within one experiment. Each experiment was repeated four times. Scale bar, 20 μm.