Prenatal caffeine damaged learning and memory in rat offspring mediated by ARs/PKA/CREB/BDNF pathway

Title:

Prenatal caffeine damaged learning and memory in rat offspring mediated by ARs/PKA/CREB/BDNF pathway

Creator:

Li, Yongmei, Zhang, Wenna, Shi, Ruixiu, Sun, Miao, Zhang, Lubo, Li, Na, and Xu, Zhice

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:94d8637e-586f-4ba7-88cf-9da7dce59bc0
uuid:94d8637e-586f-4ba7-88cf-9da7dce59bc0

Subject:

caffeine, spatial cognition, PKA, fetal growth restriction, and adenosine receptors

Type:

model:article and TEXT

Format:

bez média and svazek

Description:

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 A1 and A2A receptors, nuclear PKA Cα, Cβ 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.

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2018 Volume:67 | Number:6

Harvested from:

CDK

Metadata only:

false