Fig. 3: AMPAR-mediated currents at the Schaffer collateral synapses in vCA1 are potentiated in WT animals and not in TNF−/− mice. | Molecular Psychiatry

Fig. 3: AMPAR-mediated currents at the Schaffer collateral synapses in vCA1 are potentiated in WT animals and not in TNF−/− mice.

From: Sustained TNF signaling is required for the synaptic and anxiety-like behavioral response to acute stress

Fig. 3

A. Acute swim stress increases the AMPA/NMDA current ratio at Schaffer collateral synapses in the vCA1 at 2 and 24 h post-stress, as seen in sample traces and group data (Kruskal Wallis H(2) = 8.068, p = 0.0177; Control: n = 17, N = 11; 2 h post-stress: n = 13, N = 8; 24 h post-stress: n = 9, N = 5). B Stress potentiates the AMPA receptor (AMPAR) input-output relationship in the ventral Schaffer collaterals (24 h post-stress; two-way ANOVA of the main effect of stress F (1,40) = 11.439, p = 0.0016; control: n = 5, N = 4, stress: n = 7, N = 3). C There is no significant stress-induced potentiation of the NMDA receptor (NMDAR) mediated input-output curve in the ventral Schaffer collaterals (24 h post-stress; two-way ANOVA of the main effect of stress F (1,52) = 1 .0999, p = 0.2991; control: n = 7, N = 4, stress: n = 8, N = 4). D TNF lacking animals (TNF−/−) do not exhibit potentiation in the AMPAR currents in the ventral hippocampus in response to stress-exposure (24 h post-stress; two-way ANOVA of the main effect of stress F (1, 44) = 6.315, p = 0.0157; control: n = 6, N = 3, stress: n = 7, N = 4). *p < 0.05, **p < 0.01, ***p < 0.001. Data are presented as mean ± SEM. Sample sizes are indicated on the bar figure or in the caption.

Back to article page