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. Author manuscript; available in PMC: 2014 Aug 5.

Published in final edited form as: J Neurosci Res. 2012 Dec 26;91(3):416–425. doi: 10.1002/jnr.23155

Fig. 6 — Fig 6A: Synaptic release of acetylcholine is necessary for neuroprotection by BMI, 4R and MLA. Vesamicol (50 μM) coapplied with BMI, 4R or MLA blocked the neuroprotection. The white bars represent the NMDA controls showing the recovery of PSs after 10 min of 0.5 mM NMDA. I) The light gray bar shows the neuroprotection by 0.1 μM BMI pretreatment (N=21;*** p<0.001). The dark bar shows the inhibition of BMI neuroprotection by coapplication with vesamicol. II) Neuroprotection by 2 μM 4R (N=14;*** p<0.001) was nullified by coapplication with vesamicol. III) 10 nM MLA preapplied for 1 hour protected (N=14; *** p<0.001). Coapplication of 10 μM MLA with vesamicol inhibited the neuroprotective effect. See Fig 1 for design.

Fig 6B: Vesamicol per se did not affect NMDA neurotoxicity or the rundown of PS in the absence of NMDA. To estimate a possible enhancement of NMDA toxicity or neuroprotection by vesamicol, 0.2 mM NMDA was used. The white bar shows the decrease of PSs after application of 0.2 mM NMDA for 10 min. The gray bar reflects the effect of 1 hour application of vesamicol followed by 1 hour superfusion with ACSF and application of 0.2 mM NMDA. The comparison of the white and gray bar shows that vesamicol did not affect the toxicity of NMDA. The hatched bar shows a near complete recovery of PSs after 1 hour exposure to 50 μM vesamicol alone without later application of NMDA. The recovery of PSs in slices exposed only to vesamicol were significantly larger than in slices exposed to 0.2 mM NMDA without or with vesamicol preapplication (N=14; *; p<0.05). For design, see Fig 1.

Fig. 6 — Fig 6A: Synaptic release of acetylcholine is necessary for neuroprotection by BMI, 4R and MLA. Vesamicol (50 μM) coapplied with BMI, 4R or MLA blocked the neuroprotection. The white bars represent the NMDA controls showing the recovery of PSs after 10 min of 0.5 mM NMDA. I) The light gray bar shows the neuroprotection by 0.1 μM BMI pretreatment (N=21;*** p<0.001). The dark bar shows the inhibition of BMI neuroprotection by coapplication with vesamicol. II) Neuroprotection by 2 μM 4R (N=14;*** p<0.001) was nullified by coapplication with vesamicol. III) 10 nM MLA preapplied for 1 hour protected (N=14; *** p<0.001). Coapplication of 10 μM MLA with vesamicol inhibited the neuroprotective effect. See Fig 1 for design.

Fig 6B: Vesamicol per se did not affect NMDA neurotoxicity or the rundown of PS in the absence of NMDA. To estimate a possible enhancement of NMDA toxicity or neuroprotection by vesamicol, 0.2 mM NMDA was used. The white bar shows the decrease of PSs after application of 0.2 mM NMDA for 10 min. The gray bar reflects the effect of 1 hour application of vesamicol followed by 1 hour superfusion with ACSF and application of 0.2 mM NMDA. The comparison of the white and gray bar shows that vesamicol did not affect the toxicity of NMDA. The hatched bar shows a near complete recovery of PSs after 1 hour exposure to 50 μM vesamicol alone without later application of NMDA. The recovery of PSs in slices exposed only to vesamicol were significantly larger than in slices exposed to 0.2 mM NMDA without or with vesamicol preapplication (N=14; *; p<0.05). For design, see Fig 1.