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 vo ltage-gated Ca2+ influx in neurons examined at 2 days after the ischemic in sult (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) 2 99-306). The aim of the present study was to determine whether a similar ch ange occurs in pyramidal neurons of the CA3 region that are relatively resi stant to transient ischemia. In vitro intracellular recordings and fluorome tric Ca2+ measurements were made from CA3 neurons in coronal slices prepare d from controls and 1 or 2 days following in vivo ischemia. In slices from control and post-ischemic animals, the electrophysiological properties of C A3 neurons were consistent with significant voltage-gated Ca2+ influx, lead ing to spike frequency adaptation. Quantitative results indicated no signif icant difference in Ca2+ transients evoked by action potential trains. This Ca2+ signaling was compared with responses in CA1 neurons from the same pr eparations, which showed substantially diminished Ca2+ influx at 2 days pos t-ischemia, These findings suggest that diminished Ca2+-signaling is not a general feature of pyramidal neurons following ischemia, but is characteris tic of neurons destined to die. (C) 2000 Published by Elsevier Science irel and Ltd. All rights reserved.