Skip to main content
. 2010 Jan 25;107(6):2675–2680. doi: 10.1073/pnas.0909359107

Fig. 4.

Fig. 4.

7,8-DHF rescues a fear-expression deficit in neocortical BDNF knockouts. (A) Immunoblotting revealed that there was TrkB activation in cortical tissue after systemic 7,8-DHF administration but not with vehicle, in cortical BDNF knockout mice, or in controls. Systemic 7,8-DHF lead to phosphorylation of TrkB in cortex independently of the presence of BDNF, which is shown to be minimal in the BDNF knockout mice (anti-BDNF). (B) Average freezing to tone CS 24 h after cued fear conditioning (predrug) and again after reconditioning to a different tone (postdrug) is shown. Cre+/− had less freezing than Cre−/− (predrug). These mice were then injected (i.p.) with either 7,8-DHF or vehicle followed by reconditioning to a novel tone. Cre+/− injected with vehicle had less freezing to the new tone than did Cre−/− (*Student's t test; P < 0.05). However, Cre+/− injected with 7,8-DHF showed equivalent levels of freezing compared with 7,8-DHF–injected controls. (C) Within-training freezing during reconditioning to a new CS tone after injections of 7,8-DHF or vehicle is similar across groups. (D) When analyzing freezing 24 h after conditioning by blocks of three CS tones, Cre+/− showed diminished levels compared with Cre−/− in the absence of drug. After reconditioning with 7,8-DHF administration, Cre+/− had greater freezing compared with vehicle-injected Cre+/− but no differences compared with 7,8-DHF or vehicle-injected Cre−/− controls (*P < 0.05 versus respective Cre−/−; #P < 0.05 versus respective vehicle; n = 12 Cre-vehicle; n = 7 Cre+/− vehicle; n = 8 Cre+/− DHF; n = 7 Cre−/− DHF).