SMALL subsets Of central neurons possessing Ca2+ permeable AMPA/kainat
e channels can be identified by a histochemical stain based on kainate
-stimulated Co2+ uptake (Co2+(+) neurons) and are unusually vulnerable
to AMPA/kainate receptor-mediated injury. Using brief kainate exposur
es (which selectively destroy Co2+(+) neurons) along with kainate trig
gered Ca-45(2+) influx measurements, we estimate kainate to cause an u
nusually high rate of Ca2+ influx into Co2+(+) neurons. Also, while fu
ra-2 Ca2+ imaging revealed low (10 mu M) kainate exposures to preferen
tially induce intracellular free Ca2+ ([Ca2+](i)) elevations in Co2+() neurons, intense (100 mu M) kainate exposures used in the Ca-45(2+)
influx studies triggered comparable [Ca2+](i) rises in all neurons. Th
ese findings suggest that the exceptional vulnerability of Co2+(+) neu
rons to AMPA/kainate receptor-mediated injury reflects a high rate of
agonist triggered Ca2+ influx, and that [Ca-4(2+)](i) rises may only p
oorly reflect influx rate.