Skip to main content
. Author manuscript; available in PMC: 2010 Jun 14.
Published in final edited form as: Neuron. 2008 Jun 12;58(5):673–680. doi: 10.1016/j.neuron.2008.04.023

Fig. 3.

Fig. 3

Repeated imaging of intrinsic signal reveals that lack of TNFα signaling impairs the delayed component of plasticity induced by MD. (A, B) Average signal amplitude of the deprived-eye response (A) and open-eye response (B) in the binocular visual area, before the lid suture (pre-MD), after 2.5 – 3 days of MD (MD3), and after 5 – 6 days of MD (MD5-6) in Tnf+/+ (n=6) and Tnf−/− (n=7) mice. All data from longitudinal measurements are in the same individual animals. (C, D) Average signal amplitude of the deprived-eye response (C) and open-eye response (D) in the binocular visual area in inbred C57Bl6 wild type mice treated with cortical infusion of soluble TNF receptor1 (sTR) (n=7) or vehicle solution (n=5), before the lid suture and after 5 days of MD. Values in A–D present mean ± S.E.M of the group. **P<0.01, *P<0.05 compared with baseline (pre-MD), repeated measure ANOVA and Bonferroni multiple comparisons. (E, F) Changes in response amplitude from baseline following MD. Fractional changes in average response to deprived eye (E) and open eye (F) were calculated from measurements presented in A–D as (post-MD – pre-MD)/(pre-MD). †P<0.05 and ‡ P<0.01, paired t-test; *P<0.05 and **P<0.01, unpaired t-test. (G) Individual ODIs (circles) and mean group values (horizontal lines). The gray box presents the mean ± SD of baseline (pre-MD) ODI in Tnf+/+ animals. **P<0.01, *P<0.05 vs. corresponding baseline. (H) Response magnitude in the monocular area to the deprived eye in Tnf+/+ animals (open bar, n=6) and Tnf−/− animals (closed bar, n=6). Values present mean changes (±S.E.M.) from the baseline in response magnitude in the monocular area. **P<0.01 compared to baseline (repeated measure ANOVA), ‡ P <0.01 between groups (t-test).

HHS Vulnerability Disclosure