Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Frequent low-dose THC in adolescence disrupts microglia homeostasis and disables response to microbial infection

ABSTRACT: Frequent low-dose THC in adolescence disrupts microglia homeostasis and disables response to microbial infection

PROVIDER: PRJNA882132 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21633348_1.fastq.gz	Fastqsanger.gz
	SRR21633348_2.fastq.gz	Fastqsanger.gz
	SRR21633349_1.fastq.gz	Fastqsanger.gz
	SRR21633349_2.fastq.gz	Fastqsanger.gz
	SRR21633350_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Frequent low-dose THC in adolescence disrupts microglia homeostasis and disables response to microbial infection

Project description:Adolescence is a time of experimentation with cannabis. We evaluated whether adolescent exposure to the drug's psychotropic consituent, delta-9-tetrahydrocannabidiol (THC), might persistently alter microglia function and brain immune responses to lipopolysaccaride administration.

2022-09-22 | GSE213734 | GEO

Gene expression in the nucleus accumbens shell of adult rats of both sexes after chronic exposure to delta9-tetrahydrocannabinol during adolescence

Project description:Canabinoid exposure during adolescence alters the rewarding properties of drugs of abuse by mechanisms that are not fully understood. The nucleus accumbens is a key node of the circuit mediating the rewarding effects of most drugs. Here, we present data on the differential gene expression in the nucleus accumbens shell in male and female Wistar rats (postnatal day 90) after exposure to THC (3 mg/kg i.p.) or vehicle (ethanol:cremophor:saline; 1:1:18; 2 mL/kg i.p.) during adolescence (postnatal day 28 to postnatal day 44; injections on alternate days). There were 96 DEGs in THC-males compared to VEH-males and 87 DEGs in the females’ comparison. Only nine of these DEGs were present in both the THC vs. VEH comparison in both sexes. Our results suggest that THC exposure during adolescence affects several families of genes that have important functions for brain development, behavior and synaptic plasticity and could explain, at least in part, the complex behavioral phenotype observed in adult individuals with exposure to cannabinoids during adolescence.

2020-09-19 | GSE158188 | GEO

THC Protect

Project description:Thc protect llc

| PRJNA1097369 | ENA

In utero exposure of delta-9-tetrahydrocannabinol (THC) affects vascular transcriptome in rhesus macaques

Project description:Cannabis is commonly used in pregnancy for symptoms of nausea and pain, especially in the first trimester. Cannabis remains a federally illicit drug in the United States, but local legalization trends have resulted in increased availability and a decreased perception of harm. Unfortunately, limited scientifically rigorous information exists to inform decisions on use. Delta-9-tetrahydrocannabinol (THC, the main psychoactive component of cannabis) can cross the placenta and bind to cannabinoid receptor 1 (CB1) on the fetus. Because CB1 receptors are expressed in cardiomyocytes and endothelial cells, this suggests that THC exposure may impact fetal cardiovascular development. To understand this impact, our group used an established rhesus macaque model of chronic edible THC use during pregnancy. Animals were slowly titrated to a heavy THC dose (2.5mg/7kg/day) for 4 months preconception. Dams continued this daily THC dose throughout pregnancy with c-section delivery near term. Our model showed a decreased heart-to-body weight ratio from THC exposure. We examined the underlying changes in this selective fetal growth restriction of the cardiovascular system through tissue, protein, and gene expression analyses. H istological analysis of coronal sections of the heart and cross sections of the aorta showed no changes in collagen expression or maturity. Western blot analysis of collagen III expression showed no changes in left or right ventricle. Elastin expression was also unchanged in the aorta. To assess transcriptional changes, we performed bulk RNA-sequencing of vascular cells in the fetal aorta, umbilical vein, and umbilical artery, which revealed differentially expressed genes involved in metabolism and inflammation. These results suggest potential cardiovascular harm from in utero THC exposure by altering endothelial metabolism and inflammation.

2024-07-07 | GSE244644 | GEO

Transcription profiling of rat primary astrocytes treated with vehicle or delta-9-tetrahydrocannabinol (THC) to identify response to THC treatment

Project description:Rat primary astrocytes- were treated with vehicle or delta-9-tetrahydrocannabinol (THC), total RNA was isolated and gene expression in response to THC treatment was studied.

2006-03-05 | E-MEXP-576 | biostudies-arrayexpress

Adolescent Δ9-THC exposure and astrocyte-specific genetic vulnerability converge on NF-κB-COX-2 signaling to impair memory in adulthood

Project description:Adolescent cannabis use has been associated with long-term cognitive dysfunction attributed to action of the main cannabis ingredient, delta-9-tetrahydrocannabinol (Δ9-THC), on the cannabinoid receptor 1 (CNR1). However, not all marijuana users develop cognitive impairment, suggesting a genetic vulnerability to adverse effects of cannabis. As both neurons and glial cells express CNR1, genetic vulnerability could influence Δ9-THC-induced signaling in a cell type-specific manner. Here we use an animal model of inducible expression of dominant-negative Disrupted-In-Schizophrenia-1 (DN-DISC1) selectively in astrocytes to evaluate the molecular mechanisms whereby an astrocyte genetic vulnerability could synergistically interact with adolescent Δ9-THC exposure to impair recognition memory in adulthood. We report that selective expression of DN-DISC1 in astrocytes and adolescent treatment with Δ9-THC synergistically affected recognition memory in adult mice. Similar deficits in recognition memory were observed following knockdown of endogenous Disc1 in hippocampal astrocytes in mice treated with Δ9-THC during adolescence. At the molecular level, DN-DISC1 and Δ9-THC synergistically activated the NF-kB-COX-2 (encoded by Ptgs2 gene) pathway in astrocytes and decreased immunoreactivity of parvalbumin-positive pre-synaptic inhibitory boutons around pyramidal neurons of the CA3 area of the hippocampus. The cognitive abnormalities were prevented in DN-DISC1 mice exposed to Δ9-THC by simultaneous adolescent treatment with the COX-2 inhibitor, NS389. Our data demonstrate that individual vulnerability to cannabis can be exclusively mediated by astrocytes. Results of this work suggest that genetic predisposition within astrocytes can exaggerate Δ9-THC-produced cognitive impairments via convergent inflammatory signaling, suggesting possible targets for preventing adverse effects of cannabis within susceptible individuals.

2018-12-31 | GSE116813 | GEO

A low dose of Δ9-THC improves cognitive functions and synaptogenesis in old mice through an epigenetic mechanism

Project description:THC, the active ingredient of cannabis has been reported to impair learning and memory in humans and in laboratory animals when administered acutely. Unfortunately, most studies have been performed with young individuals although the activity of the endocannabinoid system changes during the aging process. Here we report that low doses of Δ9-THC (Delta-9-Tetrahydrocannabinol) improves learning and memory in old mice, enhances synaptic density, increases the expression of anti-ageing genes and decreases expression of pro-ageing genes in old but not in young animals. Δ9-THC elicited its beneficial effect through the CB1 receptors and increased histone acetylation was crucial for the long lasting effect. Elevation of the cannabinoid signaling may thus represent an exciting new approach to improve brain functions in old individuals.

2017-05-08 | GSE57823 | GEO

Hippocampal differential expression underlying the neuroprotective effect of delta-9-tetrahydrocannabinol (THC) microdose on old mice

Project description:Delta-9-tetrahydrocannabinol (THC) is the primary psychoactive compound of the cannabis plant and an exogenous ligand of the endocannabinoid system. In previous studies, we demonstrated that a single microdose of THC (0.002mg/kg, 3–4 orders of magnitude lower than the standard dose for rodents) exerts distinct, long-term neuroprotection in model mice subjected to acute neurological insults. When administered to old, healthy mice, the THC microdose induced remarkable long-lasting (weeks) improvement in a wide range of cognitive functions, including significant morphological and biochemical brain alterations. To elucidate the mechanisms underlying these effects, we analyzed the gene expression of hippocampal samples from the model mice. Samples taken 5 days after THC treatment showed significant differential expression of genes associated with neurogenesis and brain development. In samples taken 5 weeks after treatment, the transcriptional signature was shifted to that of neuronal differentiation and survival. This study demonstrated the use of hippocampal transcriptome profiling in uncovering the molecular basis of the atypical, anti- aging effects of THC microdose treatment in old mice.

2024-07-06 | GSE235969 | GEO

Microglial cannabinoid receptor type 1 mediates social memory deficits produced by adolescent THC exposure and 16p11.2 duplication

Project description:Adolescent cannabis use increases the risk for cognitive impairments and psychiatric disorders. Cannabinoid receptor type 1 (Cnr1) is expressed not only in neurons and astrocytes, but also in microglia, which shape synaptic connections during adolescence. Nonetheless, until now, the role of microglia in mediating the adverse cognitive effects of delta-9-tetrahydrocannabinol (THC), the principal psychoactive constituent of cannabis, has been unexplored. Here, we report that adolescent THC exposure produces microglial apoptosis in the medial prefrontal cortex (mPFC), which was exacerbated in the mouse model of 16p11.2 duplication, a representative copy number variation (CNV) risk factor for psychiatric disorders. These effects are mediated by microglial Cnr1, leading to reduction in the excitability of mPFC pyramidal-tract neurons and deficits in social memory in adulthood. Our findings highlight the importance of microglial Cnr1 to produce the adverse effect of cannabis exposure in genetically vulnerable individuals.

2023-10-03 | GSE242892 | GEO

scRNA-seq of mouse colon after THC administration

Project description:We studied the effects of delta-9-tetrhydrocannabinol (THC) on mouse colon cells, 24 hours after a single administration of THC (10mg/kg) or Vehicle (VEH) control.

2020-08-05 | GSE155669 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data