Differential regulation of mRNAs for nerve growth factor, brain-derived neurotrophic factor, and neurotrophin 3 in the adult rat brain following cerebral ischemia and hypoglycemic coma.
Open accessAbstract
In situ hybridization was used to study expression of mRNAs for members of the nerve growth factor (NGF) family in the rat brain after 2 and 10 min of forebrain ischemia and 1 and 30 min of insulin-induced hypoglycemic coma. Two hours after the ischemic insults, the level of brain-derived neurotrophic factor (BDNF) mRNA was markedly increased in the granule cells of the dentate gyrus, and at 24 h it was still significantly elevated. NGF mRNA showed a pronounced increase 4 h after 2 min of ischemia but had returned to a control level at 24 h. Both 2 and 10 min of ischemia caused a clear reduction of the level of mRNA for neurotrophin 3 (NT-3) in the dentate granule cells and in regions CA2 and medial CA1 of the hippocampus 2 and 4 h after the insults. The increase of BDNF mRNA could be partially blocked by the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist NBQX but was not influenced by the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801. Both NBQX and MK-801 attenuated the decrease of NT-3 mRNA after ischemia. One and 30 min of hypoglycemic coma also induced marked increases in BDNF and NGF mRNA in dentate granule cells with maximal levels at 2 h. If the changes of mRNA expression lead to alterations in the relative availability of neurotrophic factors, this could influence functional outcome and neuronal necrosis following ischemic and hypoglycemic insults.
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Our results show an early increase in Ngf transcription followed by its complete recovery 72 h after occlusion.
“Consistent with the data presented by Cui et al. (1999) and Lindvall et al. (1992), our results also show an early increase in Ngf transcription followed by its complete recovery 72 h after occlusion.”
From Semax and Pro-Gly-Pro activate the transcription of neurotrophins and their receptor genes after cerebral ischemia (2010) · cites this paper as Lindvall et al. 1992
The Results report increased NGF mRNA in dentate gyrus granule cells 2–4 hours after a 2-minute ischemic insult, with expression back at the control level by 24 hours. This supports the early increase and subsequent recovery, but the paper does not report a 72-hour measurement or establish recovery specifically at 72 hours after occlusion. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe downregulation of Nt-3 transcription following cerebral ischemia was confirmed by other evidence.
“This downregulation of Nt-3 transcription following cerebral ischemia was confirmed by other evidence (Lindvall et al. 1992).”
From Semax and Pro-Gly-Pro activate the transcription of neurotrophins and their receptor genes after cerebral ischemia (2010) · cites this paper as Lindvall et al. 1992
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“However, in contrast to BDNF expression, NT-3 expression level is downregulated in the adult brain by neuronal activity (Lindvall et al., 1992; Rocamora et al., 1992, 1994; Bengzon et al., 1993) (but also see Patterson et al., 1992).”
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- Authors
- Lindvall, O., Ernfors, P., Bengzon, J., Kokaia, Z., Smith, M. L., Siesjö, B. K., & Persson, H.
- Affiliations
- Skåne University Hospital (SE)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 1992-01-15
- Volume
- 89
- Issue
- 2
- Pages
- 648-652
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC48296
- OpenAlex
- W2013926808
- Cited by
- 514
- References
- 3
- Citations by year
- 2024: 2 · 2023: 4 · 2022: 6 · 2021: 1 · 2020: 6 · 2019: 4 · 2018: 5 · 2017: 2 · 2016: 12 · 2015: 9 · 2014: 7 · 2013: 7 · 2012: 4
- FWCI
- 15.14
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Funders
- National Institutes of Health (2p50ns009199-26a1)
- National Institute on Aging (AG04418, P01AG004418)
- National Institute of Neurological Disorders and Stroke (NS09199)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3, cerebral ischemia, hypoglycemic coma, insulin-induced hypoglycemia, dentate gyrus granule cells, hippocampus, AMPA receptors, NMDA receptor, NBQX, MK-801, neuronal necrosis
- MeSH terms
- Animals, Brain, Ischemic Attack, Transient, Hippocampus, Insulin Coma, Male, Nerve Growth Factors, Nerve Tissue Proteins, Nucleic Acid Hybridization, Quinoxalines, Rats, Inbred Strains, RNA, Messenger, Time Factors, Gene Expression, Dizocilpine Maleate, Proto-Oncogene Proteins c-fos, Brain-Derived Neurotrophic Factor, Neurotrophin 3, Rats
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