Secondary Activation of a Cation Conductance Is Responsible for NMDA Toxicity in Acutely Isolated Hippocampal Neurons

摘要: One of the key questions concerning glutamate toxicity is how a transient NMDA exposure can lead to delayed death neurons. To address this issue, we performed whole-cell recording on acutely isolated hippocampal CA1 neurons monitor membrane response after exposure. Transient (100 μm, 10 min) induced an inward current (postexposure current; I pe) which was associated with Ca2+- and Na+-permeable cation conductance. pe continuously increased (in absence NMDA) until neuron occurred. Application in extracellular calcium failed trigger neuronal death. Postexposure suppression protected against toxicity. These results indicate that current, by increase intracellular concentration ([Ca2+]i) itself partly carried Ca2+, links initial