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The Journal of Neurophysiology Vol. 81 No. 1 January 1999,
pp. 299-306
Copyright ©1999 The American Physiological Society
Department of Neurosciences, University of New Mexico, Albuquerque, New Mexico 87131-5223
Connor, J. A., S. Razani-Boroujerdi, A. C. Greenwood, R. J. Cormier, J. J. Petrozzino, and R.C.S. Lin. Reduced voltage-dependent Ca2+ signaling in CA1 neurons after brief ischemia in gerbils. J. Neurophysiol. 81: 299-306, 1999. An initial overload of intracellular Ca2+ plays a critical role in the delayed death of hippocampal CA1 neurons that die a few days after transient ischemia. Without direct evidence, the prevailing hypothesis has been that Ca2+ overload may recur until cell death. Here, we report the first measurements of intracellular Ca2+ in living CA1 neurons within brain slices prepared 1, 2, and 3 days after transient (5 min) ischemia. With no sign of ongoing Ca2+ overload, voltage-dependent Ca2+ transients were actually reduced after 2-3 days of reperfusion. Resting Ca2+ levels and recovery rate after loading were similar to neurons receiving no ischemic insult. The tetrodotoxin-insensitive Ca spike, normally generated by these neurons, was absent at 2 days postischemia, as was a large fraction of Ca2+-dependent spike train adaptation. These surprising findings may lead to a new perspective on delayed neuronal death and intervention.
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