Figure 4. Aβ₄₂ has a biphasic effect on KA-induced Ca²⁺ influx in primary rat cortical neuron cultures.

Cell viability assays were performed on rat primary cortical neurons using Calcein AM to investigate the toxicity of Aβ₄₂ oligomers at a range of concentrations (0.5μM, 1μM, 2.5μM, 5μM, and 10μM) after a 48 hour treatment (A). Viability data are normalized to the vehicle treated control and are presented as mean +/− SEM (n = 4, * indicates P<0.05). Rat primary cortical neurons were loaded with Fura2-PE3 and were treated with “Acute Aβ” (0.5μM Aβ₄₂ for 10 minutes) (B), “No Aβ” (C), or “Chronic Aβ” (0.5μM Aβ₄₂ for 24 hours) (D) prior to 0.5μM KA treatment. (B–D) show representative Ca²⁺_cyt traces from individual experiments in each condition. Chronic Aβ₄₂ decreased the average area under the KA-treatment portion of the Ca²⁺_cyt curve, while Acute Aβ₄₂ had the opposite effect (E). Chronic Aβ₄₂ treatment also significantly reduced the amplitude of KA-induced Ca²⁺ influx (F). Acute Aβ₄₂ increased the latency of the Ca²⁺_cyt response from control (G). Data in (D–F) are presented as mean +/− SEM from 12 to 32 separate experiments (* indicates P<0.05).