| Abstrakt: |
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. |
