Abstract:
: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.
journal_name
J Neurophysioljournal_title
Journal of neurophysiologyauthors
Connor JA,Razani-Boroujerdi S,Greenwood AC,Cormier RJ,Petrozzino JJ,Lin RCdoi
10.1152/jn.1999.81.1.299subject
Has Abstractpub_date
1999-01-01 00:00:00pages
299-306issue
1eissn
0022-3077issn
1522-1598journal_volume
81pub_type
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