Fig. 6: Involvement of CDK5 in the Preso regulation of the NMDAR-related Ca2+ response. | Cell Death & Disease

Fig. 6: Involvement of CDK5 in the Preso regulation of the NMDAR-related Ca2+ response.

From: Preso regulates NMDA receptor-mediated excitotoxicity via modulating nitric oxide and calcium responses after traumatic brain injury

Fig. 6: Involvement of CDK5 in the Preso regulation of the NMDAR-related Ca2+ response.The alternative text for this image may have been generated using AI.

Mouse cortical neuronal cultures were transfected with different lentiviruses. CDK5 activity was analyzed after traumatic neuronal injury (a). The data are presented as the mean ± SEM from five experiments. *p < 0.05 vs. LV-shCon and #p < 0.05 vs. LV-Con. After transfection with LV-Preso, the neuronal cultures were pretreated with purvalanol B (50 μM). The intracellular Ca2+ concentrations were analyzed at 12 h after TNI (b). The data are presented as the mean ± SEM from five experiments. *p < 0.05 vs. Vehicle. Mouse cortical neuronal cultures were transfected with LV-Con and LV-CDK5. The intracellular Ca2+ concentrations were analyzed at 12 h after TNI (c). The data are presented as the mean ± SEM from five experiments. *p < 0.05 vs. LV-Con. After transfection, the neuronal cultures were pretreated with DL-AP5 (100 μM). The intracellular Ca2+ concentrations were analyzed at 12 h after TNI (d). The data are presented as the mean ± SEM from five experiments. *p < 0.05 vs. Vehicle

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