Reduced Voltage-Dependent Ca2+ Signaling in CA1 Neurons After Brief Ischemia in Gerbils

John A. Connor , Seddigheh Razani-Boroujerdi , Anders C. Greenwood , Robert J. Cormier , Jeffrey J. Petrozzino , and Rick C. S. Lin Department of Neurosciences, University of New Mexico, Albuquerque, New Mexico 87131-5223 Connor, J. A., S. Razani-Boroujerdi, A. C. Greenwood, R. J. Cormier, J. J. Pet...

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Published in:Journal of neurophysiology 1999-01, Vol.81 (1), p.299-306
Main Authors: Connor, John A, Razani-Boroujerdi, Seddigheh, Greenwood, Anders C, Cormier, Robert J, Petrozzino, Jeffrey J, Lin, Rick C. S
Format: Article
Language:English
Subjects:
Action Potentials - drug effects
Animals
Brain Ischemia - physiopathology
Calcium - metabolism
Calcium Channels - drug effects
Calcium Channels - physiology
Calcium Signaling - physiology
Cerebrovascular Circulation - physiology
Electric Stimulation
Electrophysiology
Fluorescent Dyes
Fura-2
Gerbillinae
Ion Channel Gating - drug effects
Ischemic Preconditioning
Male
Microelectrodes
Neurons - physiology
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Summary:John A. Connor , Seddigheh Razani-Boroujerdi , Anders C. Greenwood , Robert J. Cormier , Jeffrey J. Petrozzino , and Rick C. S. Lin Department of Neurosciences, University of New Mexico, Albuquerque, New Mexico 87131-5223 Connor, J. A., S. Razani-Boroujerdi, A. C. Greenwood, R. J. Cormier, J. J. Petrozzino, and R.C.S. Lin. Reduced voltage-dependent Ca 2+ signaling in CA1 neurons after brief ischemia in gerbils. J. Neurophysiol. 81: 299-306, 1999. An initial overload of intracellular Ca 2+ 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 Ca 2+ overload may recur until cell death. Here, we report the first measurements of intracellular Ca 2+ in living CA1 neurons within brain slices prepared 1, 2, and 3 days after transient (5 min) ischemia. With no sign of ongoing Ca 2+ overload, voltage-dependent Ca 2+ transients were actually reduced after 2-3 days of reperfusion. Resting Ca 2+ 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 Ca 2+ -dependent spike train adaptation. These surprising findings may lead to a new perspective on delayed neuronal death and intervention.
ISSN:0022-3077
1522-1598
DOI:10.1152/jn.1999.81.1.299