PT  - JOURNAL ARTICLE
AU  - Qiang X. Chen
AU  - Katherine L. Perkins
AU  - Dennis W. Choi
AU  - Robert K. S. Wong
TI  - Secondary Activation of a Cation Conductance Is Responsible for NMDA Toxicity in Acutely Isolated Hippocampal Neurons
AID  - 10.1523/JNEUROSCI.17-11-04032.1997
DP  - 1997 Jun 01
TA  - The Journal of Neuroscience
PG  - 4032--4036
VI  - 17
IP  - 11
4099  - http://www.jneurosci.org/content/17/11/4032.short
4100  - http://www.jneurosci.org/content/17/11/4032.full
SO  - J. Neurosci.1997 Jun 01; 17
AB  - One of the key questions concerning glutamate toxicity is how a transient NMDA exposure can lead to a delayed death of neurons. To address this issue, we performed whole-cell recording on acutely isolated hippocampal CA1 neurons to monitor the membrane response after NMDA exposure. Transient NMDA exposure (100 μm, 10 min) induced an inward current (postexposure current;Ipe) which was associated with a Ca2+- and Na+-permeable cation conductance.Ipe continuously increased (in the absence of NMDA) until death of the neuron occurred. Application of NMDA in the absence of extracellular calcium failed to triggerIpe and neuronal death. Postexposure suppression of Ipe protected against NMDA toxicity. These results indicate that a cation current, which is induced by an increase in intracellular calcium concentration ([Ca2+]i) and is itself partly carried by Ca2+, links the initial NMDA exposure to neuronal death.