作者: G Chauhan , K Ray , S Sahu , K Roy , V Jain
DOI: 10.1016/J.NEUROSCIENCE.2016.09.007
关键词:
摘要: Sleep deprivation (SD) upsurges intracellular levels of adenosine, impairs adult neuronal cell proliferation (NCP) and cognition while caffeine, a non-selective adenosine A1 receptor (A1R) antagonist improves NCP during SD. We examined the selective antagonistic effects A1R using 8-cyclopentyl-1,3-dimethylxanthine (8-CPT) on impairment spatial reference memory 48h Adult male Sprague Dawley rats were sleep deprived for 48h, an automatic cage vibrating stimulus based animal activity. Spatial was tested as measure cognitive performance employing Morris Water Maze. Rats given 8-CPT dissolved in 50% dimethyl sulfoxide (DMSO), twice daily (10mg/kg, i.p.) along with 5-bromo-2-deoxyuridine (BrdU) (50mg/kg/day, i.p.). The treated showed significantly short mean latency path-length to reach platform compared SD rats. Consistent these findings, 8-CPT-treated group found have increased number BrdU, Ki-67 doublecortin (DCX) positive cells. However, no significant difference seen NeuN expression Dentate Gyrus (DG). Brain-derived neurotropic factor (BDNF) DG CA1 region observed decrease after be rescued by treatment. Furthermore, negative correlation DCX type-1 cells BDNF DG. Thus, it may concluded that treatment 8-CPT, mitigates induced decline possibly via up regulation regions.