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Long-term changes in calbindin D(28K) immunoreactivity in the rat hippocampus after cardiac arrest
Marcin Sadowski1, Jerzy W Lazarewicz, Katarzyna Jakubowska-Sadowska
1Department of Pathological Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA.
Insights
Cardiac arrest-induced ischemia caused a prolonged loss and delayed reappearance of Calbindin D(28K) (CB) in rat hippocampus. This long-term disturbance in protein expression may impair hippocampal functioning.
Area of Science:
- Neuroscience
- Cell Biology
- Pathology
Background:
- Calbindin D(28K) (CB) is a vital calcium-binding protein in the brain.
- Hippocampal function is crucial for memory and cognition.
- Ischemia can lead to neuronal damage and altered protein expression.
Purpose of the Study:
- To investigate the long-term effects of cardiac arrest-induced ischemia on CB expression in the rat hippocampus.
- To determine the timeline of CB loss and recovery following ischemic events.
- To understand the implications of altered CB expression on hippocampal function.
Main Methods:
- Analysis of Calbindin D(28K) (CB) immunoreactivity in rat hippocampus.
- Induction of 10-minute cardiac arrest-induced ischemia followed by reperfusion.
- Examination of tissue at various time points post-ischemia (3 days, 14 days, 1 month, 6 months, 12 months).
- Assessment of neuronal loss in hippocampal subfields.
Main Results:
- Complete loss of CB immunoreactivity in CA1 and CA2 pyramidal neurons within 3 days post-ischemia.
- Preserved CB immunoreactivity in the dentate gyrus, mossy fibers, and interneurons, though paler.
- Neuronal loss became apparent in CA1 stratum pyramidale from day 14 onwards.
- Delayed reappearance of CB immunoreactivity in CA1 and CA2 pyramidal neurons observed at 6 and 12 months post-ischemia.
Conclusions:
- Cardiac arrest-induced ischemia causes prolonged, long-term disturbances in hippocampal Calbindin D(28K) expression.
- The delayed recovery of CB suggests significant, lasting molecular alterations post-ischemia.
- These long-term changes in protein expression may underlie functional impairments in the hippocampus.
Abstract:
Calbindin D(28K) (CB) expression was analyzed in the rat hippocampus following 10-min-cardiac arrest-induced ischemia within a year after reperfusion. In rats examined 3 days after ischemia, CB immunoreactivity disappeared completely from CA1 pyramidal neurons and from most CA2 pyramids. In the stratum granulosum of the dentate gyrus, mossy fibers, and hippocampal interneurons, CB immunoreactivity was preserved, although staining was somewhat paler than that in control rats. A similar pattern of CB immunoreactivity was found in rats sacrificed 14 days and 1 month after cardiac arrest. From the 14th postischemic day, neuronal loss in the stratum pyramidale of CA1 but not in that of CA2 became apparent. The reappearance of CB immunoreactivity in CA1 and CA2 pyramidal neurons was noticed 6 months after ischemia, and the pattern was identical to that observed in animals sacrificed 12 months after the ictus. The prolonged loss and delayed reappearance of CB immunoreactivity in the hippocampus demonstrate that ischemia may induce long-term disturbances of protein expression, which may in turn result in impairment of hippocampal functioning.