Ontology highlight
ABSTRACT:
PROVIDER: PRJNA823521 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18635870.fastq.gz | Fastqsanger.gz | |||
| SRR18635871.fastq.gz | Fastqsanger.gz | |||
| SRR18635872.fastq.gz | Fastqsanger.gz | |||
| SRR18635873.fastq.gz | Fastqsanger.gz | |||
| SRR18635874.fastq.gz | Fastqsanger.gz |
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Project description:We established the ketamine-induced cystitis (KIC) models in female Sprague-Dawley rats. The bladder of the ketamine group and the control group were obtained to perform transcriptome analysis.
2022-02-28 | GSE189809 | GEO
Project description:Activity-dependent neuroprotective protein (ADNP) syndrome is a rare neurodevelopmental disorder caused by mutations in the ADNP gene, resulting in intellectual disability, developmental delay and autism spectrum disorder (ASD). Ketamine treatment has emerged as a promising therapeutic option for children with ADNP syndrome, showing safety and significant behavioral improvements. However, the underlying molecular perturbations caused by ketamine remain poorly described. We dissected the longitudinal effect of ketamine on the peripheral blood transcriptome of 10 individuals with ADNP syndrome. The blood transcriptome was profiled prior-to intravenous ketamine treatment (0.5mg/kg) and then again at five post-infusion timepoints: immediately post-infusion, day 1, week 1, week 2, and week 4. We show that a single low-dose infusion of ketamine triggers immediate and profound gene expression alterations, with specific enrichment of monocyte-related expression patterns. These alterations encompass diverse signaling pathways and co-expression networks, implicating up-regulation of immune and inflammatory-related processes and down-regulation of RNA processing mechanisms and metabolism. Notably, these changes exhibit a transient nature, returning to baseline levels 24 hours to 1 week after treatment. These findings advance our understanding of ketamine's molecular effects and provides a foundation for further research in elucidating its precise cellular and molecular targets. Moreover, the comprehensive assessment of ketamine-induced changes in ADNP syndrome contributes to the development of innovative therapeutic strategies for this challenging genetic disorder.
2023-07-02 | GSE235921 | GEO
Project description:We performed single cell transcriptomics analyses in medial prefrontal cortical (mPFC) and basolateral amygdala (BLA). Ketamine induced changes in inflammatory pathways reversing corticosterone effects. Cell-cell communication analyses predicted that planar-cell-polarity (PCP) signaling is decreased after corticosterone but increased following ketamine administration in excitatory neurons. Single cell transcriptomics analyses in dorsolateral prefrontal cortical (dl-PFC) neurons of depressed patients also showed decreased PCP signaling in excitatory neurons. Using chemogenetics, we found that the BLA-projecting infra limbic prefrontal cortex (IL PFC) neurons regulate immobility time in the tail suspension test and food consumption. Using RNAScope, we found, in the excitatory neurons in mPFC, Celsrs and Prickle2 were reduced by corticosterone but increased by ketamine. Using CRISPR-Cas9, we conditionally knocked out Celsrs and Prickle2 in the BLA-projecting IL-PFC neurons and found that ketamine-induced synapse restoration and behavioral remission were abolished. Ketamine affects gene expression and PCP proteins underly long-lasting effects of low-dose ketamine.
2024-06-20 | GSE191016 | GEO
Project description:To investigate ketamine-induced modifications usign C. elegans as a model
2022-12-28 | GSE215256 | GEO
Project description:Schizophrenia is often marked by poor social functioning that can have a severe impact on quality of life and independence, but the underlying neural circuity is not well understood. Here we used a translational model of subanesthetic ketamine mice to delineate neural pathways in the brain linked to social deficits in schizophrenia. Mice treated with chronic ketamine exhibit profound social and sensorimotor deficits as previously reported. Using three-dimensional c-Fos immunolabeling and volume imaging (iDISCO), we show that ketamine treatment resulted in hypoactivation of the lateral septum (LS) in response to social stimuli. Chemogenetic activation of the LS rescued social deficits after ketamine treatment, while chemogenetic inhibition of previously active populations in the LS (i.e. social engram neurons) recapitulated social deficits in ketamine-naïve mice. We then examined the translatome of LS engram neurons and found upregulation of genes encoding potassium inwardly-rectifying channels and solute transporters as well as dysregulation of genes implicated in apoptotic processes, all of which could contribute to the hypoactivation of LS social engram neurons after chronic ketamine exposure. A number of ketamine-induced differentially expressed genes (DEGs), including those involved in mitochondrial function and neuroinflammatory pathways, were shared with human schizophrenia and mouse models of neurodevelopmental disorders.
2024-08-18 | GSE241234 | GEO
Project description:Transcriptome analysis of global gene epression changes in the mouse prefrontal cortex after long term treatment with sub-aesthetics dose of ketamine.
2011-01-04 | GSE26364 | GEO
Project description:Background: Examining transcriptional regulation by existing antidepressants in key neural circuits implicated in depression, and understanding the relationship to transcriptional mechanisms of susceptibility and natural resilience, may help in the search for new therapeutics. Further, given the heterogeneity of treatment response in human populations, examining both treatment response and non-response is critical. Methods: We compared the effects of a conventional monoamine-based tricyclic antidepressant, imipramine (14 daily injections), and a rapidly acting, experimental, non-monoamine-based antidepressant, ketamine (single injection), in mice subjected to chronic social defeat stress, a validated model of depression, and used RNA-sequencing to analyze transcriptional profiles associated with susceptibility, resilience and antidepressant response and non-response in prefrontal cortex (PFC), nucleus accumbens, hippocampus, and amygdala. Results: We identified approximately equal numbers of responder and non-responder mice following ketamine or imipramine treatment. Ketamine induced more expression changes in hippocampus than other brain regions; imipramine induced more expression changes in nucleus accumbens and amygdala. Transcriptional profiles in ketamine and imipramine responders were most similar in PFC, where the least transcriptional regulation occurred for each drug. Non-response reflected both the lack of response-associated gene expression changes and unique gene regulation. In responders, both drugs reversed susceptible associated transcriptional changes as well as induced resilient associated transcription in PFC, with effects varying by drug and brain region studied. Conclusions: We generated a uniquely large resource of gene expression data in four inter-connected limbic brain regions implicated in depression and its treatment with imipramine or ketamine. Our analyses highlight the PFC as a key site of common transcriptional regulation by both antidepressant drugs and in both reversing susceptibility and inducing resilience associated molecular adaptations. In addition, we found region-specific effects of each drug suggesting both common and unique effects of imipramine versus ketamine.
2016-07-27 | GSE81672 | GEO
Project description:Prenatal exposure to synthetic corticosteroids can significantly alter postnatal development through changes in neurotransmitters and their receptors, and thus having long-lasting behavioral effects. Some of these changes have been observed in animal experiments, others also in humans prenatally exposed to synthetic corticosteroids. Here, we focused on transcriptomic changes within the prefrontal cortex of female rats prenatally exposed to either betamethasone or saline. The transcriptome has been assessed by novel computational tools to determine complex changes that may have life-long effects on phenotype, i.e., behavior. We analyzed how composition, topology and modulatory networks of the genomic fabric of the dopaminergic, GABAergic, and glutamatergic synapse (the transcriptome of the most interconnected and stably expressed gene network responsible for specific transmission) are afected by the prenatal exposure to corticosteroids and postnatal ketamine-induced seizures. One sex (F) x two prenatal exposures (B = betamethasone, S = saline) x two postnatal treatments (K = ketamine, S = saline). Biological replicates: 4 FSS, 4 FBS, 4 FBK.
2016-01-09 | E-GEOD-76694 | biostudies-arrayexpress
Project description:Patients with schizophrenia show increased striatal dopamine synthesis capacity in imaging studies. However, the mechanism underlying this is unclear but may be due to N-methyl-D-aspartate receptor (NMDAR) hypofunction and parvalbumin (PV) neuronal dysfunction leading to disinhibition of mesostriatal dopamine neurons. Here, we test this in a translational mouse imaging study using a ketamine model. Mice were treated with sub-chronic ketamine (30mg/kg) or saline followed by in-vivo positron emission tomography of striatal dopamine synthesis capacity, analogous to measures used in patients. Locomotor activity was measured using the open field test. In-vivo cell-type-specific chemogenetic approaches and pharmacological interventions were used to manipulate neuronal excitability. Immunohistochemistry and RNA sequencing were used to investigate molecular mechanisms. Sub-chronic ketamine increased striatal dopamine synthesis capacity (Cohen’s d=2.5) and locomotor activity. These effects were countered by inhibition of midbrain dopamine neurons, and by activation of cortical and ventral subiculum PV interneurons. Sub-chronic ketamine reduced PV expression in these neurons. Pharmacological intervention with SEP-363856, a novel psychotropic agent with agonism at trace amine receptor 1 (TAAR1), significantly reduced the ketamine-induced increase in dopamine synthesis capacity. These results show that sub-chronic ketamine treatment in mice mimics the dopaminergic alterations in patients with psychosis, and suggest an underlying neurocircuit involving PV interneuron hypofunction in frontal cortex and hippocampus as well as activation of midbrain dopamine neurons. A novel TAAR1 agonist reversed the dopaminergic alterations suggesting a therapeutic mechanism for targeting presynaptic dopamine dysfunction in patients.
2021-02-16 | GSE138802 | GEO
Project description:Ketamine has rapid and sustained antidepressant effects in patients with treatment resistant depression (TRD). However, the underlying mechanisms of action are not well understood. There is increasing evidence that TRD is associated with a pro-inflammatory state and that ketamine may inhibit inflammatory cytokine production. We investigated whole blood transcriptional profiles related to TRD and gene expression changes associated with treatment response to ketamine. Whole blood was collected at baseline (21 healthy controls [HC], 26 patients with TRD) and then again in patients with TRD 24 hours following a single intravenous infusion of ketamine (0.5 mg/kg). We performed RNA-sequencing and compared a) baseline transcriptional profiles between patients with TRD and HC, b) responders vs. non-responders before ketamine treatment, and c) gene expression signatures associated with clinical improvement. At baseline, patients with TRD compared to HC were characterized by a gene expression signature indicative of interferon signaling pathway activation. Prior to ketamine administration, the metabotropic glutamate receptor gene GRM2 and the ionotropic glutamate receptor gene GRIN2D were upregulated in responders compared to non-responders. Ketamine response was associated with the downregulation of multiple genes coding for pro-inflammatory cytokines, the predicted inhibition of several interferon signaling associated upstream regulators and the downregulation of Indoleamine 2,3-Dioxygenase 1 (IDO1). The current study indicates that response to ketamine may be associated with up-regulation of glutamate receptors at baseline, and linked to transcriptional changes indicative of an anti-inflammatory response following ketamine. One specific anti-inflammatory mechanism might be the downregulation of IDO1 via inhibition of the interferon pathway.
2021-10-13 | GSE185855 | GEO