인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
DBpia AI
AI 에이전트
AI 아이디어
AI 리더
AI 뷰어
Citeasy
크롬 서지관리 다운로드
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.
초록·키워드
Neonatal exposure to sevoflurane has been associated with neurodevelopmental impairments. However, the mechanisms underlying increased susceptibility to stress-related neurological disorders remain unclear. This study aimed to investigate the brain vulnerability after repeated neonatal sevoflurane exposure in rats to future traumatic stress exposure.P5 male Sprague - Dawley rats were exposed to 3% sevoflurane for 2 h daily from P6 to P8. Bumetanide, an NKCC1 inhibitor, was administered intraperitoneally before sevoflurane exposure. The expression of NKCC1 in the hippocampus at P8 was detected by reverse transcription -polymerase chain reaction and Western blot analysis. The brain vulnerability to stress exposure was assessed at P14-20 by conditioned fear traumatic stress model. The stress response was assessed by measuring serum corticosterone level. Primary hippocampal neurons of neonatal rat were cultured in vitro and exposed to sevoflurane with or without bumetanide pretreatment. The growth activity, intracellular LDH enzyme activity, ROS levels and apoptosis of hippocampal neurons were determined. Repeated neonatal sevoflurane exposure in rats enhanced serum corticosterone secretion after fear conditioning training and induced deficits in fear extinction training and recall.Pretreatment with bumetanide reversed these effects. In cultured primary neonatal rat hippocampal neurons, sevoflurane exposure enhanced the expression of NKCC1, increased the markers of neuronal cytotoxicity and downregulated the expression of Noggin, Drebrin and MAP2. In contrast, pretreatment with NKCC1 inhibitor bumetanide attenuated these adverse effects in vitro. Our results suggest repeated neonatal sevoflurane exposure enhances stress-related neurological susceptibility in rats by upregulating NKCC1, highlighting NKCC1 as a potential therapeutic target for anesthesia-induced neurodevelopmental vulnerability.
인공지능 문자 인식 모델을 통해 추출된 텍스트로, 일부 오타나 오류가 포함될 수 있으나 지속적으로 개선 중입니다.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
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