Benzodiazepines protect hippocampal neurons from degeneration after transient cerebral ischemia: an ultrastructural study
Abstract
The ability of full and partial benzodiazepine receptor agonists to prevent DNA fragmentation and neuronal death after transient cerebral ischemia was investigated in the Mongolian gerbil. Diazepam (10mg/kg, i.p.) or the partial agonist imidazenil (3mg/kg, i.p.) was administered 30 and 90min after transient forebrain ischemia produced by occlusion of the carotid arteries for 5min. Treatment with diazepam completely protected CA1b hippocampal pyramidal neurons in 94% of the animals and partially protected pyramidal neurons in 6% of the animals, as assessed with a standard Nissl stain three and four days after ischemia. DNA fragmentation was examined by the terminal dUTP nick-end labeling (TUNEL) reaction. Prior to cell death, there were no TUNEL-positive neurons in area CA1b. By three days after ischemia, when neuronal degeneration was nearly complete, 14 out of 16 gerbils exhibited a positive TUNEL reaction throughout area CA1b stratum pyramidale. In 13 out of 14 gerbils treated with diazepam, no TUNEL-positive neurons were observed in this region. Imidazenil was less effective than diazepam with respect to both neuroprotection and prevention of DNA fragmentation. Three days after ischemia, six out of eight gerbils treated with imidazenil showed partial to complete neuroprotection. Imidazenil completely prevented DNA fragmentation in only one of the animals; varying degrees of TUNEL reaction persisted in the remainder. To determine whether the neurons protected by diazepam ha…
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TSPO ligands have been shown to prevent neuronal loss in several animal models.
“TSPO ligands have been shown to prevent neuronal loss in several animal models [13;67–69].”
From Expression of the translocator protein of 18 kDa by microglia, macrophages and astrocytes based on immunohistochemical localization in abnormal human brain (2009) · cites this paper as [67]
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- Authors
- Schwartz-Bloom, R. D., Miller, K. A., Evenson, D. A., Crain, B. J., & Nadler, J. V.
- Affiliations
- Duke University (US)
- Johns Hopkins University (US)
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 2000-06
- Volume
- 98
- Issue
- 3
- Pages
- 471-484
- ISSN
- 0306-4522 (ISSN-L)
- OpenAlex
- W2086233259
- Cited by
- 80
- References
- 0
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 1 · 2022: 2 · 2020: 1 · 2018: 1 · 2017: 2 · 2016: 2 · 2014: 4 · 2013: 2 · 2012: 7
- FWCI
- 3.87
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5p50ns006233-25)
- National Institute of Neurological Disorders and Stroke (NS 28791, NS 06233, R01NS028791)
- Topics
- Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- benzodiazepines, diazepam, transient cerebral ischemia, neuroprotection, hippocampal neurons, DNA fragmentation, neurodegeneration, neuronal ultrastructure, benzodiazepine receptor agonists, Mongolian gerbil, carotid artery occlusion, TUNEL, mitochondrial swelling, dendritic degeneration
- MeSH terms
- Animals, Benzodiazepines, Ischemic Attack, Transient, Diazepam, Gerbillinae, Imidazoles, Male, Microscopy, Electron, Nerve Degeneration, Receptors, GABA-A, Apoptosis, Pyramidal Cells, Neuroprotective Agents, GABA Modulators, In Situ Nick-End Labeling, DNA Fragmentation
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