지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 저널정보
- 대한마취통증의학회(구 대한마취과학회) Korean Journal of Anesthesiology Korean Journal of Anesthesiology Vol.70 No.3
- 발행연도
- 2017.1
- 수록면
- 335 - 340 (6page)
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초록· 키워드
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Background: Neonatal exposure to anesthetics induces neuronal apoptosis and long-term cognitive dysfunction in rodents. We showed that the nicotinamide adenine dinucleotide phosphate-oxidase inhibitor apocynin not only reduces neurotoxicity by decreasing superoxide levels and preventing mitochondrial dysfunction but also improves long-term memory impairment in neonatal mice exposed to sevoflurane. We also found that after the contextual fear conditioning test, glutamatergic neurons expressed c-Fos (neural activation) regardless of previous exposure to sevoflurane. Moreover, there were fewer c-Fos-expressing glutamatergic neurons in the basolateral amygdala (BLA) after exposure to sevoflurane than after exposure to carrier gas. In this study, we investigated whether the administration of apocynin prior to sevoflurane exposure would preserve glutamatergic neurons in the BLA. Methods: Apocynin (50 mg/kg) was injected intraperitoneally into six-day-old male mice 30 min before 6 h of exposure to 3% sevoflurane or carrier gas only. The mice were allowed to mature and then were subjected to the contextual fear conditioning test. The neural activation and neuron population in the BLA were investigated 2 h later. Results: Administration of apocynin prior to neonatal sevoflurane exposure not only prevented learning deficits but also preserved c-Fos-expressing glutamatergic neurons in the BLA. Conclusions: Apocynin mitigates the cognitive impairment induced by neonatal sevoflurane exposure and preserves c- Fos-expressing glutamatergic neurons in the basolateral amygdala.
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참고문헌 (23)
참고문헌 신청
Jevtovic-Todorovic V / 2003 / Early exposure to common anesthetic agents causes widespread neurodegeneration in the developing rat brain and persistent learning deficits / J Neurosci 23:876~882
Young C / 2005 / Potential of ketamine and midazolam, individually or in combination, to induce apoptotic neurodegeneration in the infant mouse brain / Br J Pharmacol 146:189~197
Brambrink AM / 2010 / Isoflurane-induced neuroapoptosis in the neonatal rhesus macaque brain / Anesthesiology 112:834~841
Zheng H / 2013 / Sevoflurane anesthesia in pregnant mice induces neurotoxicity in fetal and offspring mice / Anesthesiology 118:516~526
Satomoto M / 2009 / Neonatal exposure to sevoflurane induces abnormal social behaviors and deficits in fear conditioning in mice / Anesthesiology 110:628~637
Young C / 2005 / Potential of ketamine and midazolam, individually or in combination, to induce apoptotic neurodegeneration in the infant mouse brain / Br J Pharmacol 146:189~197
Brambrink AM / 2010 / Isoflurane-induced neuroapoptosis in the neonatal rhesus macaque brain / Anesthesiology 112:834~841
Zheng H / 2013 / Sevoflurane anesthesia in pregnant mice induces neurotoxicity in fetal and offspring mice / Anesthesiology 118:516~526
Satomoto M / 2009 / Neonatal exposure to sevoflurane induces abnormal social behaviors and deficits in fear conditioning in mice / Anesthesiology 110:628~637
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