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Prenatal caffeine damaged learning and memory in rat offspring mediated by ARs/PKA/CREB/BDNF pathway
Y. Li, W. Zhang, R. Shi, M. Sun, L. Zhang, N. Li, Z. Xu
Jazyk angličtina Země Česko
Typ dokumentu časopisecké články
NLK
Directory of Open Access Journals
od 1991
Free Medical Journals
od 1998
ProQuest Central
od 2005-01-01
Medline Complete (EBSCOhost)
od 2006-01-01
Nursing & Allied Health Database (ProQuest)
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 1998
- MeSH
- bludiště - učení účinky léků fyziologie MeSH
- kofein toxicita MeSH
- krysa rodu rattus MeSH
- mozkový neurotrofický faktor metabolismus MeSH
- paměť účinky léků fyziologie MeSH
- poruchy paměti chemicky indukované diagnóza metabolismus MeSH
- potkani Sprague-Dawley MeSH
- protein vázající cAMP responzivní element metabolismus MeSH
- proteinkinasy závislé na cyklickém AMP metabolismus MeSH
- purinergní receptory P1 metabolismus MeSH
- signální transdukce účinky léků fyziologie MeSH
- těhotenství MeSH
- zpožděný efekt prenatální expozice chemicky indukované diagnóza metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- těhotenství MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
Prenatal exposure to caffeine can cause developmental problems. This study determined chronic influence of prenatal caffeine at relatively higher doses on cognitive functions in the rat offspring. Pregnant Sprague-Dawley rats (4-month-old) were exposed to caffeine (20 mg/kg, twice a day) for whole pregnancy from gestational day 4. Fetal and offspring body and brain weight was measured. Learning and memory were tested in adult offspring with Morris water maze. Learning and memory-related receptors were measured. The exposure to prenatal caffeine not only caused fetal growth restriction, but also showed long-term effects on learning and memory in the offspring. The caffeine offspring exhibited longer escape latency and path length in navigation testing. The number of passing the target was significantly reduced in those offspring. The expression of adenosine A(1) and A(2A) receptors, nuclear PKA C(alpha), C(beta) subunits, and pCREB were significantly increased in the fetal and neonatal brain, and suppressed in the hippocampus of the adult offspring. The expression of BDNF and TrkB were reduced regardless of various ages. The results suggest that intrauterine programming dysfunction of adenosine receptors and the down-stream of cAMP/PKA/pCREB system may play an important role in prenatal caffeine induced cognition disorders in the adult offspring.
Center for Perinatal Biology Loma Linda University CA USA
Institute for Fetology 1st Hospital of Soochow University Suzhou China
Citace poskytuje Crossref.org
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