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Fig. 3 | Journal of Neuroinflammation

Fig. 3

From: Oxidative stress and inflammation cause auditory system damage via glial cell activation and dysregulated expression of gap junction proteins in an experimental model of styrene-induced oto/neurotoxicity

Fig. 3

Morphological and functional damage induced by the oto/neurotoxic insult in the auditory cortex (ACx). A Graph shows results of field excitatory post-synaptic potential (fEPSP) amplitude measured following stimulation of afferent fibers in ACx layer II/III at increasing intensities. Statistical analysis by two-way ANOVA followed by Tukey’s post-hoc revealed significant differences between groups (p < 0.001; n = 17 slices from 4 Styrene and n = 16 slices from 4 Ctrl rats). B–E Representative images of Golgi-stained segments from apical (B, D) and basal dendrites (C, E) of pyramidal neurons of layers II/III in Ctrl and Styrene groups. Scale bar: 10 μm. F Bar graphs showing values of spine density in apical and basal dendrites of neurons of layer II/III of the ACx in the experimental groups (n = at least 30 segments from 30 different neurons were analyzed from three animals/groups; two-way ANOVA, apical dendrites p < 0.0001, basal dendrites p < 0.0001). G, H Images of western immunoblot indicating lower pGluA1Ser845 (G) and higher cleaved caspase-3 (H) levels in the ACx of styrene-treated rats compared to controls. Histograms show densitometric analyses in all samples normalized to total protein amount (GluA1 and GAPDH/Caspase-3) (n = 3 animals for each group; Student’s t test, pGluA1 p = 0.022; Caspase-3 p = 0.0004). Data are expressed as mean ± SEM. Asterisks indicate statistical significance (*p < 0.05; ***p < 0.001)

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