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. 1996 Jul 1;16(13):4069–4079. doi: 10.1523/JNEUROSCI.16-13-04069.1996

Fig. 5.

Fig. 5.

Kainate injury to the spinal motor neuronal population is Ca2+-dependent. A, Kainate injury to large SMI-32(+) and peripherin(+) neurons is Ca2+-dependent. Cultures were exposed to kainate (100 μm for 10 min) in the presence of the indicated Ca2+ concentration. Overall neuronal loss and loss of large SMI-32(+) or peripherin(+) neurons were evaluated 20–24 hr later (as described in Materials and Methods). Values represent mean ± SEM compiled from four experiments;n = 9–15 cultures per condition. & indicates labeled neuronal loss significantly different from labeled neuronal loss seen in the 1.8 mmCa2+ condition (p < 0.05 by two-tailed t test). # indicates labeled neuronal loss significantly different from total neuronal loss after the same exposure (p < 0.01 by two-tailedt test). B, Kainate-induced loss of spinal cord ChAT activity is Ca2+-dependent. Cultures were exposed to kainate (100 μm for 15 min) in the presence of the indicated Ca2+ concentration. Overall neuronal loss and loss of ChAT activity were assessed 20–24 hr later (as described). Values represent mean ± SEM compiled from 10 experiments; n = 27–36 cultures for each condition.& indicates ChAT activity loss significantly different from that seen in the 10 mm Ca2+condition (p < 0.01 by two-tailed ttest). # indicates ChAT activity loss significantly different from overall neuronal injury after the same exposure (p < 0.01 by two-tailed t test).