Sensitivity of the developing rat brain to hypobaric/ischemic damage parallels sensitivity to N-methyl-aspartate neurotoxicity
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The endogenous excitotoxin, glutamate (Glu), acting at the N-methyl- aspartate (NMA) subtype of Glu receptor, is thought to play a major role in hypoxic/ischemic neuronal degeneration. In the present study, the sensitivities of the developing rat CNS to hypoxic/ischemic neuronal degeneration and to the neurotoxic action of NMA were compared at various postnatal ages. In the hypoxic/ischemic experiments, ischemia was produced by unilateral common carotid artery ligation and hypoxia by subjecting the pups to a partial vacuum. Keeping the duration of the hypobaric episode constant at 75 min for all age groups, we observed that the vulnerability of the immature brain to hypobaric/ischemic damage increased during the early neonatal period (days 2–4), reached a peak at day 6 and then diminished progressively with increasing age. In the second part of the study, NMA was microinjected unilaterally into the head of the caudate nucleus at various postnatal ages (2–80 d). In the early neonatal period (days 2– 6), injections of relatively small doses of NMA (6–15 nmol) produced a dose-dependent widespread excitotoxic reaction throughout the forebrain with peak sensitivity being observed on day 6. The cytotoxic reaction to NMA was identical in appearance and time course to that induced by hypobaric/ischemic methods. With increasing age, the excitotoxic response to a given dose of NMA decreased progressively and the lesions became more strictly confined to the injection site. Cell populations most sensitive to NMA toxicity in the 2–10 d period closely correlated with those most vulnerable to hypoxia/ischemia, and sensitivity to both types of injury reached a peak at 6 d. These findings reinforce other evidence linking an excitotoxic mechanism and the NMA subtype of Glu receptor to hypoxic/ischemic brain damage and suggest that there may be a period during development when NMA receptors are hypersensitive to excitotoxic stimulation, thus rendering the neurons possessing such receptors hypervulnerable to hypoxic/ischemic damage.
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Exposure to NMDA antagonist, ethanol, or general anesthetics causes a significant increase in neuronal degeneration at P6-P7.
“For instance, exposure to N-methyl-D-aspartate (NMDA) antagonist, ethanol, or general anesthetics, causes a significant increase in neuronal degeneration at P6–P7456.”
From Transient blockade of ERK phosphorylation in the critical period causes autistic phenotypes as an adult in mice (2015) · cites this paper as [4]
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- Authors
- Ikonomidou, C., Mosinger, J., Salles, K., Labruyere, J., & Olney, J.
- Affiliations
- Washington University in St. Louis (US)
- ORCID
- Ikonomidou, C
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1989-08-01
- Volume
- 9
- Issue
- 8
- Pages
- 2809-2818
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6569702
- OpenAlex
- W1534709134
- Cited by
- 332
- References
- 33
- Citations by year
- 2026: 1 · 2024: 2 · 2022: 2 · 2021: 4 · 2020: 2 · 2019: 2 · 2018: 3 · 2017: 4 · 2016: 5 · 2015: 8 · 2014: 12 · 2013: 5 · 2012: 8
- FWCI
- 18.15
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Mental Health (MH-38894)
- National Institute of Environmental Health Sciences (ES 07066)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD 24237)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal and fetal brain pathology
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- excitotoxicity, hypobaric hypoxia, cerebral ischemia, hypoxic-ischemic brain injury, glutamate receptors, developing brain, postnatal age, neurotoxicity, caudate nucleus, neuronal vulnerability, neonatal period
- MeSH terms
- Air Pressure, Animals, Animals, Newborn, Aspartic Acid, Atmospheric Pressure, Brain, Brain Ischemia, Disease Susceptibility, Microinjections, Nerve Degeneration, Neurons, Rats, Inbred Strains, N-Methylaspartate, Rats
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