Fig. 3
From: Vesicular glutamate release from central axons contributes to myelin damage
White matter ischemic glutamate release is primarily vesicular. a Ischemia-evoked [glutamate]e elevation in adult rat RON is Na+-independent/TBOA-insensitive. b The ischemic-[glutamate]e rise is Ca2+-dependent (ANOVA with Holm−ŠÃdák post test: P = 0.012) and diltiazem-sensitive (P = 0.010). c, d In juvenile rat RON, the ischemic [glutamate]e elevation (P = 0.001 vs., control aCSF) is Ca2+-dependent (P = 0.009 vs., ischemia)/Na+-independent and resistant to inhibitors of non-vesicular glutamate release pathways. e, f Ischemic-[glutamate]e elevation in juvenile RON is significantly inhibited by blockers of vesicular glutamate loading bafilomycin (P = 0.004); rose bengal (P = 0.013) and combined bafilomycin + TBOA (P = 0.004)
