Sleep is an evolutionarily conserved physiological process implicated in the consolidation of learning and memory (L/M). Here, we hypothesize that sleep deprivation (SD)-induced cognitive deficits in zebrafish and mouse are mediated through reduction in O-GlcNAcylation in the brain. At the molecular level, SD downregulated mRNA of key enzymes of HBP metabolism and O-GlcNAc transferase (OGT) along with increased O-GlcNAcase (OGA) expression. Fear conditioning (FC) induced an increase in the expression or activities of proteins associated with long term memory (LTM), and at the same time, OGT protein and O-GlcNAcylation were significantly increased in the normalbut not in the SD-group of zebrafish. Suppression of HBP by the GFAT inhibitor, diazo-oxo-norleucine (DON), impaired L/M function and FC-mediated activation of PKA/CREB signaling. Conversely, enhancement of HBP by glucosamine significantly restored cognitive deficits and increased PKA/CREB signaling in the SD group. To our knowledge, the current study has provided valuable insights into the molecular and biochemical changes associated with L/M at the whole-brain level using the zebrafish and mouse system for the first time. Our findings highlight the role of the HBP during the L/M process and provide potential therapeutic targets for cognitive defects.
본 학회는 화학, 생화학, 분자생물학, 미생물학, 식품공학, 의학, 약학, 유전공학 및 생물공학, 환경 및 기타 공업 등 전 분야의 탄수화물관련 이론과 기술을 연구 발전시키고 산학협동을 통해 이를 보급하여 국내 관련 산업의 발전 및 국민생활의 과학화에 기여하고자 하며, 이러한 목표와 비젼의 실현을 위해 회원들이 적극적인 참여와 활동을 전개하고자 한다.
간행물
간행물명
한국당과학회 학술대회
간기
연간
수록기간
2006~2022
십진분류
KDC 517DDC 614
이 권호 내 다른 논문 / 한국당과학회 학술대회 2020 한국당과학회 연례학술대회(온라인)