Secondary Ca2+ overload indicates early neuronal injury which precedes staining with viability indicators.
Spinal neurons, lethally challenged with excitatory amino acids (EAAs) or with high-K+, underwent a biphasic rise in free intracellular calcium concentration ([Ca2+]i). In contrast to the initial rise in [Ca2+]i which recovered, the secondary, irreversible [Ca2+]i increase was unaffected by antagonists of EAA receptors or Ca2+ channels. Also, it correlated highly with cell death, but preceded vital staining with trypan blue and ethidium homodimer, reflecting damaged cellular Ca2+ regulation rather than plasma membrane leakiness. Our findings suggest that delayed Ca2+ overload is the end-product rather than the cause of Ca(2+)-triggered neurotoxic processes.
Tymianski
M
M
Playfair Neuroscience Unit, Toronto Hospital, Ont., Canada.
Charlton
M P
MP
Carlen
P L
PL
Tator
C H
CH
D000596:Amino Acids / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D002470:Cell Survival / Q000187:drug effects; D005260:Female; D006651:Histocytochemistry; D051379:Mice; D008856:Microscopy, Fluorescence; D009474:Neurons / Q000187:drug effects*; D011247:Pregnancy; D013116:Spinal Cord / Q000166:cytology / Q000187:drug effects; D013194:Staining and Labeling
D000596:Amino Acids; D002118:Calcium