Dr. Aizenman’s laboratory has established that the liberation of intracellular zinc following an oxidative stimulus can lead to activation MAPK pathways. In one scenario, p38 activation leads to an enhancement of voltage-gated potassium currents, which precedes caspase activation. In other circumstances, zinc can also lead to ERK activation and cell death as a result of PARP overactivation.

In other studies, Dr. Aizenman's laboratory has observed that caspase 3 needs to be activated to induce tolerance in ischemic preconditioning. This unexpected finding suggests that pathways normally activated during cell death programs may also be important in signaling the neuron to upregulate endogenous neuroprotective strategies. Zinc has been recently found to also be important in this process. zinc

Students in the laboratory will be exposed to molecular biological techniques, cell culture, protein biochemistry, immunostaining, confocal microscopy, and in vitro neurotoxicity methods. In collaboration with Karl Kandler, we are also using fluorescence imaging to detect changes in intracellular zinc.