Continuous ethanol treatment of embryos reduced expression of the mature neural and photoreceptor markers elavl3/huC, rho, and crx; in addition, expression of the neural and retinal progenitor markers ascl1b and pax6b was maintained at the undifferentiated stage, indicating that retinal and CNS neural progenitor cells failed Tideglusib mouse to undergo further differentiation.

Moreover, ethanol treatment enhanced BrdU incorporation, histone H3 phosphorylation, and paw expression in neural progenitor cells, thereby maintaining a high rate of proliferation. Ethanol treatment also resulted in sustained transcription of ccnd1/cyclin D1 and ccne/cyclin E throughout development in neural progenitor cells, without an appropriate increase of cdkn1b/p27 and cdkn1c/p57 expression, suggesting that these cells failed to exit from the cell cycle. Although NAC was able to mitigate ethanol-mediated apoptosis, it was unable to ameliorate the defects in visual and CNS neural differentiation, suggesting that abrogated neural development in ethanol-exposed embryos is unlikely to arise from excessive

apoptosis. In conclusion, we demonstrate that the pathological effect of ethanol on zebrafish embryos is partially attributable to cell death and inhibition of visual and CNS neuron differentiation. Excessive apoptosis largely results from the accumulation of ROS, whereas abrogated neural development is caused by failure of cell cycle arrest, which in turn prevents a successful transition from proliferation to differentiation.

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“Creativity is a cornerstone Protein Tyrosine Kinase inhibitor of what makes us human, yet the neural mechanisms underlying creative thinking are poorly understood. A recent surge of interest into the neural underpinnings of creative behavior has produced a banquet of data that is tantalizing but, considered as a whole, deeply self-contradictory. We review the emerging literature and take stock of several long-standing theories and widely held beliefs about creativity. A total of 72 experiments, reported in 63 articles, make up the core of the review. They broadly fall into 3 categories: divergent thinking, artistic creativity, and insight. Electroencephalographic studies of divergent thinking yield highly variegated results. YAP-TEAD Inhibitor 1 Neuroimaging studies of this paradigm also indicate no reliable changes above and beyond diffuse prefrontal activation. These findings call into question the usefulness of the divergent thinking construct in the search for the neural basis of creativity. A similarly inconclusive picture emerges for studies of artistic performance, except that this paradigm also often yields activation of motor and temporoparietal regions. Neuroelectric and imaging studies of insight are more consistent, reflecting changes in anterior cingulate cortex and prefrontal areas.