Ca2+ signaling in gerbil CA3 hippocampal neurons following transient in vivo ischemia.

Using the gerbil model of post-ischemic neuron death in the hippocampal CA1 region, it was recently shown that there is a strong down-regulation of voltage-gated Ca2+ influx in neurons examined at 2 days after the ischemic insult (Connor, J.A., Razani-Boroujerdi, S., Greenwood, A.C., Cormier, R.J., Petrozzino, J.J. and Lin, R.C., Reduced voltage-dependent Ca2+ signaling in CA1 neurons after brief ischemia in gerbils, J. Neurophysiol., 81 (1999) 299-306). The aim of the present study was to determine whether a similar change occurs in pyramidal neurons of the CA3 region that are relatively resistant to transient ischemia. In vitro intracellular recordings and fluorometric Ca2+ measurements were made from CA3 neurons in coronal slices prepared from controls and 1 or 2 days following in vivo ischemia. In slices from control and post-ischemic animals, the electrophysiological properties of CA3 neurons were consistent with significant voltage-gated Ca2+ influx, leading to spike frequency adaptation. Quantitative results indicated no significant difference in Ca2+ transients evoked by action potential trains. This Ca2+ signaling was compared with responses in CA1 neurons from the same preparations, which showed substantially diminished Ca2+ influx at 2 days post-ischemia. These findings suggest that diminished Ca2+-signaling is not a general feature of pyramidal neurons following ischemia, but is characteristic of neurons destined to die.