FIGURE 6.

GSK3 inhibition increases hippocampal levels of phospho‐Ser831 GluA1, synapsin‐1 and BDNF proteins in male Tg26 mice. (a) Representative western blots and densitometricanalyses showing the effect of saline and GSK3 inhibitor (TDZD‐8; 5 mg·kg⁻¹ for 24 h) treatments on hippocampal total GSK3β (46 kDa) and phospho‐Ser9‐GSK3β (46 kDa; inactive form) proteins in male WT and Tg26 mice (n = 7 per group for saline and TDZD‐8 treated WT; n = 5 per group for saline and TDZD‐8 treated Tg26). Analysis of the phospho‐Ser9‐GSK3β/GSK3β ratios showed a significant increase in both male WT and Tg26 mice following TDZD‐8 treatment. *P < 0.05, unpaired Student'st‐test. Analysis of total GSK3β/GAPDH ratios showed similar levels between saline and TDZD‐8 treated mice. GAPDH (37 kDa) served as loading control. (b) Representative western blots and densitometricanalyses showing the effect of saline and TDZD‐8 treatments on hippocampal levels of phospho‐Ser831 GluA1 (106 kDa; n = 8 per group for saline treated WT, n = 9 per group for TDZD‐8 treated WT, n = 6 per group for saline treated Tg26, n = 6 per group for TDZD‐8 treated Tg26) and synapsin‐1 (77 kDa; n = 6 per treatment group for WT and Tg26) proteins in male WT and Tg26 mice. Pan‐Cadherin (140 kDa) and β‐actin (42 kDa) served as loading controls. *P < 0.05, as compared to saline‐treated mice, unpaired Student's t‐test. (c)ELISA analysis of hippocampal BDNF proteins in male WT and Tg26 mice following saline and TDZD‐8 treatments (n = 4 per treatment group for WT and n = 8 per treatment group for Tg26). *P < 0.05, as compared to saline‐treated mice, unpaired Student's t‐test. (d) qRT‐PCR analysis of hippocampal HIV‐1 long terminal repeat (LTR) mRNA in saline and TDZD‐8 treated male Tg26 mice (n = 8 per treatment group)