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Original Article
- eNOS Gene Polymorphisms in Perinatal Hypoxic-Ischemic Encephalopathy.
- Min Cho, Kwang Sun Hyun, David Chanwook Chung, In Young Choi, Myeung Ju Kim, Young Pyo Chang
- Korean J Pathol. 2009;43(4):306-311.
- DOI: https://doi.org/10.4132/KoreanJPathol.2009.43.4.306
- Retraction in: J Pathol Transl Med 2019;53(5):345
- 65,535 View
- 15,403 Download
- 1 Crossref
In Vitro
- The Effects of Excitatory Amino Acids and Their Receptors on Neuronal Damage of Rat Brain in Hypoxic-Ischemic Encephalopathy.
- Heasoo Koo
- Korean J Pathol. 1995;29(5):545-562.
- 1,575 View
- 10 Download
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Abstract
- Since the role of excitatory amino acids such as glutamate and aspartate and their receptors mediating cellular injury through various mechanisms were known in hypoxic-ischemic injury and associated diseases of central nervous system, blocking agents for transmitter release or receptors have been tried to reduce the cellular damages and subsequent sequelae experimentally. Several in vitro studies suggested two kinds of glutamate neurotoxicity: (1) rapid toxicity due to influx of sodium or chloride with resultant cellular edema and consequent damage, which is associated with N-methyl-D-Aspartate(NMDA) as well as non-NMDA receptors, (2) calcium mediated delayed toxicity associated mainly with NMDA receptor. This study was conducted to investigate the role of rapid toxicity in hypoxic-ischemic injury. Early lesions of 30 minutes to 24 hours after hypoxic-ischemic insult were examined by autoradiography with radiolabelled glutamate and kainitic acid (KA) as well as light and electron microscopy. Late changes were evaluated on formaldehyde-acetic acid-methanol(FAM) fixed brain 1 week after the insult. Cornus ammonis(CA) l of hippocampus showed the highest density of NMDA receptors, which was decreased constantly from 2 hours to 24 hours. In contrast, CA3 of hippocampus showed the highest density of KA receptors, which was the lowest at 6 hour and increased thereafter. Light microscopic examination showed the worst changes during 30 minutes to 6 hours. After 1 week, most of the cases showed degeneration of neurons and CAI and CA3 did not show the difference. Electron microscopic examination showed marked degenerative changes of neurons as well as neuropils starting from 30 minutes after the insult. In conclusion, rapid toxicity mediated by non-NMDA(KA) receptor seen in CA3 lead to permanent damage in 1 week old lesion.
Original Article
- Effects of Calcitriol on Delayed Neuronal Damage of Hippocampus in Transient Global Ischemia Model of Mature Gerbil.
- Hye Jin Park, Hea Soo Koo, Woon Sup Han, Kyung Kyu Choi
- Korean J Pathol. 2003;37(5):307-315.
- 1,685 View
- 16 Download
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Abstract
PDF - BACKGROUND
It is well documented that calcium ions perform a major role in neuronal degeneration in cerebrovascular disease and the other degenerative diseases, and that 1,25-dihydroxyvitamin D3 (D3) has the dose-dependent protective effects. This study was performed to examine the effects of different D3 dosages against delayed neuronal damage of the hippocampus.
METHODS
Mature mongolian gerbils were injected with either 0.8 microgram/kg/day (group 2) for 5 days or 1.0 microgram/kg/day for 8 days (group 3) prior to the 10 min ligation of the bilateral common carotid arteries. Immunohistochemical expression for the glial cell line-derived neurotrophic factor (GDNF), the basic fibroblast growth factor (bFGF) and the platelet-derived neurotrophic factor (PDNF) was observed in the D3-injected (0.8 microgram/kg/day for 5 days) group.
RESULTS
Group 2 showed a highly significant attenuation of delayed neuronal damage in the lateral CA1 region at 7 days after reperfusion. Group 3 showed unilateral or bilateral hemispheric infarcts 24 h after the onset of reperfusion. The D3-injected group showed a markedly increased bFGF expression level.
CONCLUSION
The dose-dependent effect of D3 suggests the importance of determining the appropriate D3 dose for clinical applications. Although the mechanism(s) of neuroprotection by D3 remains unclear, D3 may facilitate a reduction in ischemia-induced oxidative stress via the activation of the neurotrophic factors, including bFGF and GDNF.
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