Memory deficits are commonly observed in patients following cardiac arrest and hippocampal CA1 neurons are exquisitely sensitive to ischemia, making them a logical cell type to study following global cerebral ischemia. In addition to various neuroprotective strategies being studied in the laboratory, we are interested in assessing the effects of global ischemia on long-term potentiation (LTP) of Schaffer collateral to CA1 synapses in the hippocampus, a well characterized form of synaptic learning that is likely impaired following global ischemia. We are currently performing field recordings to measure LTP in hippocampal slices from mice that have undergone CA/CPR. By combining this method with neurobehavioral measures of hippocampal learning we will gain insight into the mechanisms that lead to memory deficits. We are particularly interested in how ion channel modulation affects plasticity and outcome following an ischemic insult. We have identified calcium activated potassium channels (SK2) as a target for neuroprotection and are investigated how inhibition or potentiation of this channel alters plasticity after cardiac arrest.