Objective To explore the difference of sleep quality and the influencing factors in ketamine dependent subjects and methamphetamine dependent subjects.Methods 60 ketamine dependent subjects and 60 methamphetamine dependent subjects with Pittsburgh sleep quality index (PSQI),self-rating depression scale (SDS),self-rating anxiety scale (SAS) were tested.Results Methamphetamine dependent subjects was significantly more likely to elicit poor sleep quality than ketamine dependent subjects (P =0.022).The sleep quality of ketamine dependent subjects had a positive correlation with anxiety(P =0.015),depression(P =0.038),the onset age (P =0.029),and the dose of ketamine use in the last three months (P =0.048),while the sleep quality of methamphetamine dependent subjects had a positive correlation with the total time of ketamine use (P =0.038),anxiety (P =0.041),the dose of ketamine use in the last three months (P =0.011).Conclusion Methamphetamine dependent subjects are prone to a more serious poor sleep quality than ketamine dependent subjects.

The self-renewal and multipotent potentials in neural stem cells (NSCs) maintain the normal physiological functions of central nervous system (CNS). The abnormal differentiation of NSCs would lead to CNS disorders. However, the mechanisms of how NSCs differentiate into astrocytes, oligodendrocytes (OLs) and neurons are still unclear, which is mainly due to the complexity of differentiation processes and the limitation of the cell separation method. In this study, we modeled the dynamics of neural cell interactions in a systemic approach by mining the high-throughput genomic and proteomic data, and identified 8615 genes that are involved in various biological processes and functions with significant changes during the differentiation processes. A total of 1559 genes are specifically expressed in neural cells, in which 242 genes are NSC specific, 215 are astrocyte specific, 551 are OL specific, and 563 are neuron specific. In addition, we proposed 57 transcriptional regulators specifically expressed in NSCs may play essential roles in the development courses. These findings provide more comprehensive analysis for better understanding the endogenous mechanisms of NSC fate determination.
Animals ; Astrocytes ; cytology ; metabolism ; Cell Differentiation ; genetics ; Gene Expression Profiling ; Gene Regulatory Networks ; Mice ; Neural Stem Cells ; cytology ; metabolism ; Oligodendroglia ; cytology ; metabolism ; Protein Interaction Mapping

The visual system plays an important role in our daily life. In this study, we found that loss of dendritic cell factor 1 (DCF1) in the primary visual cortex (V1) caused a sight deficit in mice and induced an abnormal increase in glutamic acid decarboxylase 67, an enzyme that catalyzes the decarboxylation of glutamate to gamma aminobutyric acid and CO, particularly in layer 5. In vivo electrophysiological recordings confirmed a decrease in delta, theta, and beta oscillation power in DCF1-knockout mice. This study presents a previously unknown function of DCF1 in V1, suggests an unknown contact between DCF1 and GABA systems, and provides insight into the mechanism and treatment of visual deficits.
Animals ; Brain Waves ; genetics ; Disease Models, Animal ; Electroencephalography ; Gene Expression Regulation ; drug effects ; genetics ; Geniculate Bodies ; drug effects ; metabolism ; Ginkgolides ; therapeutic use ; Glutamate Decarboxylase ; metabolism ; Lactones ; therapeutic use ; Membrane Proteins ; deficiency ; genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nerve Tissue Proteins ; deficiency ; genetics ; Photic Stimulation ; Proto-Oncogene Proteins c-fos ; metabolism ; Vision Disorders ; drug therapy ; genetics ; pathology ; physiopathology ; Visual Cortex ; metabolism ; pathology ; gamma-Aminobutyric Acid ; metabolism