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. 2010 Sep 13;107(39):17005–17010. doi: 10.1073/pnas.1008938107

Fig. 5.

Fig. 5.

BDNF reexpression in SCs rescues vestibular function and synapse formation in GFAP-DN-erbB4 mice. (A) BDNF immunostaining of P26 utricular, maculae from control (BDNFstop), GFAP-DN-erbB4 mice carrying the BDNFstop transgene, and mice carrying all three transgenes (GFAP-DN-erbB4, BDNFstop and PLP/CreERT) show that tamoxifen increases BDNF expression in SCs of the utricular macula of BDNFstop::GFAP-DN-erbB4::PLP/CreERT mice to levels similar to those of control mice. (Scale bar, 20 μm.) Box plot analysis of VsEP thresholds: arrow illustrates the threshold shift in GFAP-DN-erbB4 mice, which had no response at the highest levels tested (ND, not detectable) (B) and peak 1 amplitudes at 5 dB (C) from control mice (n = 6), GFAP-DN-erbB4 mice carrying the BDNFstop transgene (n = 6), and mice carrying all three transgenes (n = 4) show that conditional overexpression of BDNF rescues the vestibular function of GFAP-DN-erbB4 mice at P26. Magnitude of the evoking head jerk is expressed in dB re: 1.0 g/ms; ***P < 0.0001. (D) Quantification of synapses (colocalized RIBEYE and GluR2/3), presynaptic ribbons (RIBEYE puncta), and postsynaptic receptor plaques (GluR2/3 puncta) in utricular maculae of the same mice tested in A–C shows that BDNF overexpression in SCs rescues the synaptic loss in GFAP-DN-erbB4 mice; ***P < 0.0001. Error bars in D represent SEMs.