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- Cerebellar Hippocampal and Basal Nuclei Transient Edema with Restricted diffusion (CHANTER) syndrome due to antidepressant
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Sangun Nah, Han Bit Kim, Sangsoo Han, Sungwoo Choi, Hoon Lim
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J Korean Soc Clin Toxicol. 2022;20(1):31-34. Published online June 30, 2022
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DOI: https://doi.org/10.22537/jksct.2022.20.1.31
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Abstract
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- Cerebellar Hippocampal and Basal Nuclei Transient Edema with Restricted diffusion (CHANTER) syndrome is characterized by an altered mental status. The acute MRI lesions show abnormal restricted diffusion imaging bilaterally and symmetrically in the cerebellum, hippocampus, and basal nuclei. This syndrome is an unknown syndrome and is presumed to be mainly an opioidinduced toxidrome. Here, we present a case study wherein we show that it can also be caused by an antidepressant overdose.
- Effects of N-acetylcystein on changes in parvalbumin-positive interneurons in the hippocampus after carbon monoxide poisoning
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Seon Tae Kim, Su Jin Yoo
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J Korean Soc Clin Toxicol. 2021;19(2):100-109. Published online December 31, 2021
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DOI: https://doi.org/10.22537/jksct.2021.19.2.100
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Abstract
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- Purpose: The purpose of this study was to investigate effect of N-acetylcysteine (NAC) on the injury of putative parvalbumin positive interneurons defined by molecular marker and hippocampal long-term potentiation (LTP), a marker of neural plasticity following acute carbon monoxide (CO) poisoning. Methods: Adult Sprague-Dawley rats were exposed to 1100 ppm CO for 40 minutes followed by 3000 ppm CO for 20 minutes. Animals received daily intraperitoneal injection of NAC (150 mg/kg) for 5 days after CO exposure. Changes in learning and spatial memory were evaluated by Y-maze test 5 days after the poisoning. In vivo LTP in hippocampal CA1 area was evaluated by using extracellular electrophysiological technique. Immunohistochemical staining were adopted to observe expressional damages of parvalbumin (PV) immunoreactive interneurons in the hippocampus following the poisoning. Results: Acute CO intoxication resulted in no changes in memory performance at Y-maze test but a significant reduction of LTP in the in hippocampal CA1 area. There was also a significant reduction of PV (+) interneurons in the hippocampal CA1 area 5 days after CO poisoning. Daily treatment of NAC significantly improved hippocampal LTP impairment and reduced immunoreactivity for PV in the hippocampus following the acute CO poisoning. Conclusion: The results of this study suggest that reduction of hippocampal LTP and PV (+) interneurons in the hippocampus is sensitive indicator for brain injury and daily NAC injections can be the alternative therapeutics for the injury induced by acute CO poisoning.
- Application of Thallium Autometallography for Observation of Changes in Excitability of Rodent Brain following Acute Carbon Monoxide Intoxication
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Min Soo Lee, Seung Bum Yang, Jun Ho Heo
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J Korean Soc Clin Toxicol. 2019;17(2):66-78. Published online December 31, 2019
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DOI: https://doi.org/10.22537/jksct.2019.17.2.66
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Abstract
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- Purpose: Thallium (TI+) autometallography is often used for the imaging of neuronal metabolic activity in the rodent brain under various pathophysiologic conditions. The purpose of this study was to apply a thallium autometallographic technique to observe changes in neuronal activity in the forebrain of rats following acute carbon monoxide (CO) intoxication. Methods: In order to induce acute CO intoxication, adult Sprague-Dawley rats were exposed to 1100 ppm of CO for 40 minutes, followed by 3000 ppm of CO for 20 minutes. Animals were sacrificed at 30 minutes and 5 days after induction of acute CO intoxication for thallium autometallography. Immunohistochemical staining and toluidine blue staining were performed to observe cellular damage in the forebrain following intoxication. Results: Acute CO intoxication resulted in significant reduction of TI+ uptake in major forebrain structures, including the cortex, hippocampus, thalamus, and striatum. In the cortex and hippocampal CA1 area, marked reduction of TI+ uptake was observed in the cell bodies and dendrites of pyramidal neurons at 30 minutes following acute CO intoxication. There was also strong uptake of TI+ in astrocytes in the hippocampal CA3 area following acute CO intoxication. However, there were no significant histological findings of cell death and no reduction of NeuN (+) neuronal populations in the cortex and hippocampus at 5 days after acute CO intoxication. Conclusion: The results of this study suggest that thallium autometallography can be a new and useful technique for imaging functional changes in neural activity of the forebrain structure following mild to moderate CO intoxication.