Fig. 6.

Disrupting F-actin has no impact on excitotixicity or neuronal Ca²⁺ loading evoked by exogenous NMDA or l-glutamate. Cultured cortical neurons were pretreated with the indicated concentrations of latrunculin-A (0–5 μm) or cytochalasin-D (0–30 μm) before undergoing exposure to 0, 30, or 100 μm NMDA (A, B) or 10–1000 μml-glutamate (C) for 60 min (in 2 μm nimodipine and 10 μm CNQX; see Materials and Methods). The cultures were then maintained for a further 23 hr to measure neuronal survival (A1–C1) or used for⁴⁵Ca²⁺ accumulation measurements (A2–C2). A, Effects of treatment with latrunculin-A on NMDAR-mediated excitotoxicity (A1) and⁴⁵Ca²⁺ loading (A2).B, Effects of treatment with cytochalasin-D on NMDAR-mediated excitotoxicity (B1) and⁴⁵Ca²⁺ loading (B2).C, Effect of treatment with 1 μmlatrunculin-A on glutamate-mediated excitotoxicity (C1) and ⁴⁵Ca²⁺ accumulation (C2). Symbols in A1 andB1 represent the mean survival (± SE) of 4–64 cultures per experimental condition, obtained from at least two (usually 4–6) different platings. The lines indicate the least-squares linear regression curves obtained for each NMDA concentration.Columns in A2 and B2represent the mean (± SE) ⁴⁵Ca²⁺accumulation averaged from 16–36 cultures obtained from 4–6 different culture platings. Columns in C1 and C2were obtained from 16 cultures per condition pooled from two separate platings. Error bars are shown where they exceed symbol size.