Journal article
Experimental Brain Injury Induces Regionally Distinct Apoptosis during the Acute and Delayed Post-Traumatic Period
The Journal of neuroscience, v 18(15), pp 5663-5672
01 Aug 1998
PMID: 9671657
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
The temporal pattern of apoptosis in the adult rat brain after lateral fluid-percussion (FP) brain injury was characterized using terminal deoxynucleotidyl-transferase-mediated biotin-dUTP nick end labeling (TUNEL) histochemistry and agarose gel electrophoresis. Male Sprague Dawley rats were subjected to brain injury and killed for histological analysis at intervals from 12 hr to 2 months after injury (
n
= 3/time point). Sham (uninjured) controls were subjected to anesthesia with (
n
= 3) or without (
n
= 3) surgery. Apoptotic TUNEL-positive cells were defined using stringent morphological criteria including nuclear shrinkage and fragmentation and condensation of chromatin and cytoplasm. Double-labeled immunocytochemistry was performed to identify TUNEL-positive neurons (anti-neurofilament monoclonal antibody RM044), astrocytes (anti-glial fibrillary acidic protein polyclonal antibody), and oligodendrocytes (anti-cyclic nucleotide phosphohydrolase polyclonal antibody). Compared with that seen with sham controls, in the injured cortex, significant apoptosis occurred at 24 hr (65 ± 19 cells;
p
< 0.05) with a second, more pronounced response at 1 week after injury (91 ± 24 cells;
p
< 0.05). The number of apoptotic cells in the white matter was increased as early as 12 hr after injury and peaked by 1 week (33 ± 6 cells;
p
< 0.05). An increase in apoptotic cells was observed in the hippocampus at 48 hr (13 ± 8), whereas in the thalamus, the apoptotic response was delayed, peaking at 2 weeks after injury (151 ± 71 cells;
p
< 0.05). By 2 months, the number of apoptotic cells in most regions had returned to uninjured levels. At 24 hr after injury, TUNEL-labeled neurons and oligodendrocytes were localized primarily to injured cortex. By 1 week after injury, populations of TUNEL-labeled astrocytes and oligodendrocytes were present in the injured cortex, while double-labeled neurons were present predominantly in injured cortex and thalamus, with a few scattered in the hippocampus. DNA agarose gels confirmed morphological identification of apoptosis. These data suggest that the apoptotic response to trauma is regionally distinct and may be involved in both acute and delayed patterns of cell death.
Metrics
Details
- Title
- Experimental Brain Injury Induces Regionally Distinct Apoptosis during the Acute and Delayed Post-Traumatic Period
- Creators
- Alana C. Conti - University of PennsylvaniaRamesh Raghupathi - University of PennsylvaniaJohn Q. Trojanowski - University of PennsylvaniaTracy K. McIntosh - Departments of Neurosurgery and
- Publication Details
- The Journal of neuroscience, v 18(15), pp 5663-5672
- Publisher
- Society for Neuroscience
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Neurobiology and Anatomy
- Web of Science ID
- WOS:000074971800011
- Scopus ID
- 2-s2.0-0032146787
- Other Identifier
- 991019222773704721
UN Sustainable Development Goals (SDGs)
This publication has contributed to the advancement of the following goals:
InCites Highlights
Data related to this publication, from InCites Benchmarking & Analytics tool:
- Web of Science research areas
- Neurosciences