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. Author manuscript; available in PMC: 2023 Aug 1.
Published in final edited form as: Biol Psychiatry. 2021 Dec 15;92(3):216–226. doi: 10.1016/j.biopsych.2021.11.024

Figure 5.

Figure 5.

Restoration of synaptic strength by MRK-016 is absent in mice lacking GABAAR α5 subunits. (A) Representative traces showing larger AMPA:NMDA ratios in wildtype animals compared to α5 KOs. (B) CMMS decreases TA-CA1 synaptic strength. Among stress-sensitive wildtype mice, 3mg/kg MRK-016 (n=6 animals) significantly increased AMPA:NMDA ratios compared to vehicle (n=5) treated animals (p=0.0045). AMPA:NMDA ratios in stress-sensitive α5 KO mice were not significantly different between vehicle (n=6) or MRK-016 (n=6) groups (p=0.7749). Wildtype mice displayed significantly higher AMPA:NMDA ratios than α5 KO mice after MRK-016 administration (p=0.0044). Two-way ANOVA indicated significant interaction of genotype × MRK-016 (F 1,19 = 11.62, P=0.0029). (C) MRK-016 increases the AMPA-mediated component of the TA-CA1 fEPSP in stress-sensitive wildtype but not α5 KO mice (n=individual slices from Fig. 5B, p=0.0079). One-way ANOVA indicated significant effect of treatment on AMPAR-mediated slope (F 3,75 = 4.211, P=0.0083). (D) MRK-016 administration does not change the NMDAR-mediated component of the TA-CA1 fEPSP. One-way ANOVA indicated no effect of treatment on NMDAR-mediated slope (F 3,75 = 1.476, P=0.2279). (E) TA-CA1 synaptic strength correlates with an animal’s sucrose preference (n=23, r=0.6625, p=0.0006. Line of fit: Y = 3.791*X + 33.20). (F) TA-CA1 synaptic strength positively trends with an animal’s female urine sniffing preference (n=23, r=0.2481, p=0.2536. Line of fit: Y = 1.637*X + 37.66). p<0.01 **p<0.005 ***, ns: not significant.