Temporal Profile of
Ultrastructural Changes in Cortical Neurons after a Compression
Lesion
B. ANDERSSON1,2, B. BJELKE1,
E. SYKOVÁ2,3
1Department of Clinical Neuroscience, Karolinska
Institute, Stockholm, Sweden, 2Institute of
Experimental Medicine AS CR, Prague and 3Department
of Neuroscience, Second Medical Faculty, Charles University,
Prague, Czech Republic
Received October 25, 2004
Accepted July 18, 2005
On-line available August 5, 2005
Summary
We studied the occurrence of apoptosis and secondary delayed
cell death at various time points in the penumbra zone, which is
the target for therapeutic intervention after stroke. A
compression lesion was induced in the right sensory motor cortex
of rat brains. At 0.5, 1, 3, 6, 12, 24, 48 and 72 h after
lesioning, motor functions were evaluated by behavioral tests,
and cortical layers IV and V were examined by electron
microscopy. Behavioral recovery was observed at 48 h after
lesioning. At 0.5-1 h in the lesioned area, the neuropil was
expanded and contained affected cells. Apoptotic cells were
found between 0.5-72 h, and at 12 h, 47.3 % of the total cell
number was apoptotic cells. On the contralateral side, cells
showed an enlarged endoplasmic reticulum at 3 h, indicating
secondary delayed cell death. Our results show that a
compression lesion is a useful model for studying
ultrastructural changes in injured cells. The lesion results in
the penumbra zone with apoptotic cell death between 0.5-72 h. As
secondary delayed cell death occurred on the contralateral side
at three hours after lesioning might be the time period during
which injured, but still viable, neurons can be targets for
acute treatment.
Key words
Stroke • Ischemia • Sensory motor cortex • Cell death •
Ultrastructure
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