Transcriptome analysis of the hippocampus in late postnatal mice after repeated ketamine anesthesia
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ABSTRACT:
PROVIDER: PRJNA734265 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14699819_1.fastq.gz | Fastqsanger.gz | |||
| SRR14699819_2.fastq.gz | Fastqsanger.gz | |||
| SRR14699820_1.fastq.gz | Fastqsanger.gz | |||
| SRR14699820_2.fastq.gz | Fastqsanger.gz | |||
| SRR14699821_1.fastq.gz | Fastqsanger.gz |
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Project description:Numerous recent studies showed that early anesthesia during neurodevelopment may induce changes in specific behaviors. We further studied the effects of early anesthetic exposures regarding addiction behavior later in life. Postnatal day (PND) 16 C57BL/6 mice received ketamine anesthesia for 5 consecutive days. Addiction behavior was evaluated 1 week after anesthesia treatment. Neurological changes after repeated anesthesia were evaluated using high-performance liquid chromatography, RNA sequencing, electrophysiology studies. Repeated ketamine anesthesia during the critical neurodevelopment period increased the expression of genes involved with action potential, and induced excitatory/inhibitory (E/I) imbalance in hippocampal CA1 pyramidal neurons of male mice. Such neurological changes were associated with increases in drug-induced contextual addiction memory.
2022-07-14 | GSE175894 | GEO
Project description:Transient hypoxia in pregnancy stimulates a physiological reflex response that redistributes blood flow and defends oxygen delivery to the fetal brain. The chemoreceptor reflex that is responsible for this physiological response is dependent on glutamatergic neurotransmission which, in times of vigorous activity, could produce cell death secondary to calcium uptake. We designed the present experiment to test the hypotheses that transient hypoxia produces damage of the hippocampus and that ketamine, an antagonist of NMDA receptors, reduces the damage. Late-gestation, chronically catheterized fetal sheep were subjected to a 30 min period of ventilatory hypoxia that decreased fetal PaO2 from 17±1 to 10±1 mm Hg, or normoxia (PaO2 17±1 mm Hg), with or without pretreatment (10 min before hypoxia/normoxia) with ketamine (3 mg/kg, iv). One day (24 h) after hypoxia/normoxia, fetal hippocampus was removed and mRNA extracted for transcriptomics and systems biology analysis. Hypoxia stimulated a transcriptomics response consistent with a an increase in inflammation (e.g., cytokine binding and response to LPS). Ketamine pretreatment reduced these responses. The inflammation response modeled with transcriptomic system biology was validated by immunohistochemistry and showed increased abundance of microglia/macrophages after hypoxia in the hippocampal tissue that ketamine significantly reduced. We conclude that transient hypoxia produces inflammation of the fetal hippocampus and that ketamine, in a standard clinical dose, reduces the inflammation response.
2017-08-31 | GSE97916 | GEO
Project description:Acute fetal hypoxia is a form of fetal stress that stimulates renal vasoconstriction and ischemia as a consequence of the physiological redistribution of combined ventricular output. We have demonstrated that hypoxia in late ovine gestation induces inflammation in the brain that is ameliorated by treatment with ketamine. We hypothesized that the fetal kidney would also respond to hypoxia with an increase in the expression of inflammatory genes, and that ketamine (an N-Methyl-D-aspartate receptor antagonist) would reduce or block this response. Enriched biological processes for the 427 upregulated genes were immune and inflammatory responses and for the 946 down-regulated genes were metabolic processes. Ketamine countered the effects of hypoxia on upregulated immune/inflammatory responses as well as the down-regulated metabolic responses. We conclude that our transcriptomics modeling predicts that hypoxia activates inflammatory pathways and reduces metabolism in the fetal kidney cortex, and ketamine blocks or ameliorates this response. The results suggest that ketamine may have therapeutic potential for protection from ischemic renal damage.
2016-09-01 | GSE66920 | GEO
Project description:Ketamine has been found to elicit a rapid antidepressant effects in treatment-refractory affective disorders. To indicate the underlying mechanism of action we have performed whole-genome microarray profiling. Moreover, the effects of ketamine were compared to other NMDA receptor antagonists phencyclidine and memantine. Type: Drug response, Time-course, Gene expression profiling with Illumina Microarrays Keywords: Ketamine, NMDA antagonist, Phencyclidyne, Memantine, Time-course, Gene Expression, Acute treatment
2015-12-31 | GSE73798 | GEO
Project description:Acute fetal hypoxia is a form of fetal stress that stimulates renal vasoconstriction and ischemia as a consequence of the physiological redistribution of combined ventricular output. We have demonstrated that hypoxia in late ovine gestation induces inflammation in the brain that is ameliorated by treatment with ketamine. We hypothesized that the fetal kidney would also respond to hypoxia with an increase in the expression of inflammatory genes, and that ketamine (an N-Methyl-D-aspartate receptor antagonist) would reduce or block this response. Enriched biological processes for the 427 upregulated genes were immune and inflammatory responses and for the 946 down-regulated genes were metabolic processes. Ketamine countered the effects of hypoxia on upregulated immune/inflammatory responses as well as the down-regulated metabolic responses. We conclude that our transcriptomics modeling predicts that hypoxia activates inflammatory pathways and reduces metabolism in the fetal kidney cortex, and ketamine blocks or ameliorates this response. The results suggest that ketamine may have therapeutic potential for protection from ischemic renal damage. At the time of surgery, fetuses were randomly assigned to one of the four groups (n=3-4/group): normoxic control, normoxia+ketamine, hypoxic control, and hypoxia+ketamine. Hypoxia was induced for 30 min in chronically catheterized fetal sheep (125±3 d; term=145-147d), with or without ketamine (3 mg/kg) administered intravenously to the fetus 10 min prior to hypoxia. Fetuses were euthanized 24 hours after the onset of hypoxia, and the kidney cortex were collected for RNA extraction and gene array studies. Gene expression was analyzed using ovine Agilent 15.5 k array and validated with qPCR. Significant differences in gene expression between groups were determined with t-statistics using the limma package for R (Pâ¤0.05).
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Project description:RNA sequencing of young mice hippocampus after anesthesia
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Project description:Proper brain wiring relies on the precise distribution of axonal projections to specific subcellular domains of their target neurons. These spatially confined connections establish the anatomical foundation for neural circuit assembly. The mossy fiber (MF)–CA3 pathway in the hippocampus is an excellent system to study the mechanisms underlying lamina-specific connectivity. In rodents, MF projections develop postnatally and reach their mature configuration by the end of the second postnatal week. MF axons synapse on the proximal segments of the dendrites but avoid the somas of CA3 pyramidal neurons. As dentate gyrus granule neurons are continuously generated and integrated into the existing hippocampal circuit throughout the postnatal period and adulthood, the mechanisms that guide MF axons to achieve lamina-specific targeting of these later-born granule neurons remain unclear. Here, we show that deletion of the neurodevelopmental disorder-associated protein capicua (CIC) results in abnormal MF targeting in the mouse hippocampus. Notably, this defect emerges after the second postnatal week and persists into adulthood, distinguishing it from classical MF guidance defects, which typically manifest during the first postnatal week. We also demonstrate that this miswiring is due to CIC loss in dentate gyrus granule neurons rather than CA3 pyramidal neurons. Single-nucleus transcriptomics and trajectory analysis reveal a loss of a mature granule neuron subtype and dysregulation of axon guidance genes that are normally downregulated as granule neurons mature. Our findings uncover a previously unrecognized role for CIC in hippocampus development and offer insights into the regulation of lamina-specific MF connectivity in the postnatal brain.
2025-09-23 | GSE280854 | GEO
Project description:Ketamine has been found to elicit a rapid antidepressant effects in treatment-refractory affective disorders. To indicate the underlying mechanism of action we have performed whole-genome microarray profiling. Moreover, the effects of ketamine were compared to other NMDA receptor antagonists phencyclidine and memantine. Type: Drug response, Time-course, Gene expression profiling with Illumina Microarrays Keywords: Ketamine, NMDA antagonist, Phencyclidyne, Memantine, Time-course, Gene Expression, Acute treatment The microarray experiment was performed to analyze time-course of drug-induced transcriptional response in C57BL/6J mouse hippocampus. Three NMDA antagonists (ketamine 20 mg/kg, phencyclidine 5 mg/kg and memantine 15 mg/kg i.p.) were selected for the comparison. Drug doses were based on the literature. To analyze dynamics of early, intermediate and relatively late changes of mRNA abundance the experiment was performed in four time points (1, 2, 4 and 8h after drug administration). To exclude influence of drug injection and circadian rhythm on gene expression profile, control groups of saline treated and naive animals were prepared for each time point. Samples from 2 mice were pooled per microarray, 3 biological replicates were used per time point and 12 arrays per each drug. To provide appropriate balance in the whole dataset groups were equally divided between the array hybridization batches. 'Complete' normalized data and non-normalized data (containing control rows not represented in Platform GPL6105) are linked below as supplementary files.
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Project description:To reveal influence of anesthesia in toxicogenomics study, gene expression analysis of liver of Sprague-Dawley rat after isoflurane anesthesia or CO2/O2 anesthesia was performed. The liver samples were excised from each rat after isoflurane anesthesia or CO2/O2 anesthesia. The gene expression profiles in liver were measureed by Agilent microarray.
2015-07-24 | GSE71277 | GEO
Project description:Long noncoding RNAs (lncRNAs) play important roles in brain function modulation and neurodegenerative diseases. However, whether lncRNA regulations are involved in the mechanisms of perioperative neurocognitive disorders (PNCD), especially in anesthesia related brain dysfunction, remains unknown. We explored the expression and regulation pattern profiles of lncRNAs in the hippocampus of aged rats after sevoflurane anesthesia with microarrays.
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