Journal: Neurobiology of disease
Article Title: Neonatal hypoxia-ischemia alters the events governing the hippocampal critical period of postnatal synaptic plasticity leading to deficits in working memory in mice
doi: 10.1016/j.nbd.2024.106722
Figure Lengend Snippet: Hybrid box and whiskers with column scatter plots represent the distribution of (A) the BDNF levels (pg/g of protein) (B1 & B2) α-fodrin 150 kDa and 120 kDa breakdown products relative to 250 kDa total and (D1) GFAP fold change relative to sham, for sham (white), NT (dark grey) and TH (light grey) at P11, P15, P18 and P40. *, p = 0.05 vs. sham (KW ANOVA with Dunn-Bonferroni post hoc). Representative blots with loading control showed for α-fodrin ( B ) and GFAP (D2) . Scatter plot with best-fit-curve represent (C) α-fodrin 150/250 kDa ( x-axis ) vs. BDNF level ( y-axis ) and (E) GFAP fold-change ( x-axis ) vs. BDNF level ( y-axis ). Best-fit regression line is depicted in continuous black line and 95 % CI limits by discontinuous lines. BDNF , brain derived neurotrophic factor; NT , normothermia; S , Sham; TH , Therapeutic hypothermia.
Article Snippet: For assessment of brain injury, we followed the methods described above and sections were exposed to the following primary antibodies: 1) α-fodrin (Enzo Life Sciences, Farmingdale NY, USA, FG6090; RRID: AB_2050678) mouse monoclonal IgG1 antibody raised against chicken blood cell membranes following hypotonic lysis and mechanical enucleation (0.25 μg/mL), detecting bands at 250, ~150, and ~ 120 kDa and 2) GFAP (ProteinTech, 16,825–1-AP; RRID: AB_2109646) rabbit polyclonal IgG antibody raised against GFAP fusion protein (ProteinTECH, Ag10423) (0.2 μg/mL), detecting a band at ~50 kDa.
Techniques: Control, Derivative Assay