Project description:We demonstrate that high fat diet (HFD)-induced obesity alters the transcriptional state of lateral hypothalamic glutamate neurons in mice.
Project description:This SuperSeries is composed of the following subset Series:; GSE2039: FACS purified cortical projection neurons; GSE17783: Analysis of gene expression in FACS-purified cortical projection neurons using Affymetrix 430 2.0 microarrays Experiment Overall Design: Refer to individual Series
Project description:The addition of Glutamate to the lens induced by galactose eliminated the white clouding formed and showed a therapeutic effect. Genes regulated by Glutamate addition were identified by microarray analysis. A total of seven samples were used in this analysis: two samples without galactose (control), three samples with galactose (galactose) and two samples with Glutamate (Glutamate).
Project description:The lateral hypothalamic area (LHA) regulates feeding- and reward-related behavior, but because of its molecular and anatomical heterogeneity, the functions of defined neuronal populations are largely unclear. Glutamatergic neurons within the LHA (LHAVglut2) negatively regulate feeding and appetitive behavior. However, this population comprises transcriptionally distinct and functionally diverse neurons that project to diverse brain regions, including the lateral habenula (LHb) and ventral tegmental area (VTA). To resolve the function of distinct LHAVglut2 populations, we systematically compared projections to the LHb and VTA using viral tracing, single-cell sequencing, electrophysiology, and in vivo calcium imaging. LHAVglut2 neurons projecting to the LHb or VTA are anatomically, transcriptionally, electrophysiologically, and functionally distinct. While both populations encode appetitive and aversive stimuli, LHb projecting neurons are especially sensitive to satiety state and feeding hormones. These data illuminate the functional heterogeneity of LHAVglut2 neurons, suggesting that reward and aversion are differentially processed in divergent efferent pathways.
Project description:Ciprofloxacin, an inhibitor of bacterial gyrase and topoisomerase IV, was shown to inhibit growth of C. glutamicum with concomitant excretion of L-glutamate. C. glutamicum strains overproducing L-lysine, L-arginine, L-ornithine, and putrescine, respectively, produced L-glutamate instead of the desired amino acid when exposed to ciprofloxacin. Even in the absence of the putative L-glutamate exporter gene yggB, ciprofloxacin effectively triggered L-glutamate production. When C. glutamicum wild type was cultivated under nitrogen-limiting conditions, 2-oxoglutarate rather than L-glutamate was produced as consequence of exposure to ciprofloxacin. Transcriptome analysis revealed that ciprofloxacin increased RNA levels of genes involved in DNA synthesis, repair and modification. Enzyme assays showed that 2-oxoglutarate dehydrogenase activity was decreased due to ciprofloxacin addition. Here, it was shown for the first time that production of L-glutamate by C. glutamicum may be triggered by an inhibitor of DNA synthesis and L-glutamate titers of up to 37 ± 1 mM and a substrate specific L-glutamate yield of 0.13 g/g were reached.
Project description:Glutamate, a major neurotransmitter in the mammalian nervous sytem, has been involved in the mediation of excitotoxicity commonly observed in the pathogenesis of stroke. Current study focused on gaining an insight into the molecular mechanisms of glutamate-induced neuronal death A total of 15 RNA samples were analyzed. There is one treatment conditions of 250uM glutamate. 3 replicates were collected for each of the selected time-points (5h, 15h and 24h) in addition to 6 replicates of shared vehicle control.
Project description:We profiled populations of mouse neurons in the Anterior Lateral Motor (ALM) cortex, as defined by retrograde projection labeling. For each sample, we injected one of four regions (thalamus, IRN in medulla, superior colliculus, or pons) using the retrograde virus rAAV2-retro with a fluorescent repoter, and collected cells in the ALM whose projections to the target area were labelled. 50-120 cells were collected from each injection experiment and then profiled using standard bulk RNA-seq protocols
Project description:Glutamate is a major excitatory neurotransmitter in the nervous system. Increased and persistent release of glutamate is toxic to neurons and this excitotoxicity is a hallmark of several neurodegenerative diseases. Here, we use GRO-seq to screen for the acute transcriptional changes induced by glutamate exposure on embryonic mouse cortical neurons to reveal downstream molecules which could participate in glutamate-induced toxicity. We show that several miRNA genes, such as miR-21, have altered expression upon glutamate exposure.