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. 2019 Dec 4;39(49):9852–9863. doi: 10.1523/JNEUROSCI.0886-19.2019

Figure 3.

Figure 3.

Fmr1 deletion in VGlut1-expressing glutamatergic neurons is neither sufficient nor necessary for recapitulating the AGS phenotype. A, tdTomato fluorescence in spiral ganglion neurons in the cochlea from vGlut1Cre/+:Rosa26 tdTomato/+ mice indicating Cre expression in these cells. B–D, AGS data for mice derived from vGlut1Cre/+ and Fmr1cOFF/y cross-breeding. Deletion in cortex does not result in a change in AGS measurements compared with WT controls. E–G, Data from vGlut1Cre/+ and Fmr1cON/y cross-breeding. AGS measurements resulting from Cre-dependent Fmr1 expression are no different from the cON-KO control and increased compared with WT controls. N values for AGS data were as follows: cOFF = 16, 14, 18, and 14; cON = 14, 15, 19, and 17. *p < 0.05, ***p < 0.001. K-W ANOVA followed by Dunn's test.