Exercise-mimetic AICAR transiently benefits brain function.

摘要: Exercise enhances learning and memory in animals humans. The role of peripheral factors that may trigger the beneficial effects running on brain function has been sparsely examined. In particular, it is unknown whether AMP-kinase (AMPK) activation muscle can predict enhancement plasticity. Here we compare administration AMPK agonist 5-Aminoimidazole-4-carboxamide 1-β-D-ribofuranoside (AICAR, 500 mg/kg), for 3, 7 or 14 days one-month-old male C57BL/6J mice, signaling. At time-points where observed equivalent running- AICAR-induced pAMPK levels (7 days), cell proliferation, synaptic plasticity gene expression, as well markers oxidative stress inflammation dentate gyrus (DG) hippocampus lateral entorhinal cortex (LEC) were evaluated. 7-day time-point, both regimens increased new DG number brain-derived neurotrophic factor (BDNF) protein levels. Furthermore, microarray analysis LEC tissue showed a remarkable overlap between AICAR regulation neuronal, mitochondrial metabolism related classes. Interestingly, while similar outcomes treatments stable over time muscle, an inversion occurred at fourteen days. compound no longer proliferation neurotrophin levels, upregulated expression apoptotic genes inflammatory cytokine interleukin-1β. Thus, exercise mimetic produces changes consistent with those does not have same sustainable positive brain, indicating only consistently benefits function.