Transcription profiling of brain tissue from mice after safety or fear conditioning
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Daniela Pollak
PROVIDER: E-MEXP-1358 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Gene expression profiling following different learning paradigms may help in defining the moleular pathways of memory formation. In this study we analyzed the gene expression pattern of murine hippocampus at different time points (0.5 h, 2h, 6h) after trace fear conditioning. We compared trained mice with naive mice that remained in their homecages. Keywords: Time course We used 3 arrays for each experimental condition. Each array was hybridized witha a pool of RNA of 6 animals.
2010-05-27 | E-GEOD-16158 | biostudies-arrayexpress
Project description:Here we tested a hypothesis that epileptogenesis influences expression pattern of genes in the basolateral amygdala that are critical for fear conditioning. Whole genome molecular profiling of basolateral rat amygdala was performed to compare the transcriptome changes underlying fear learning in epileptogenic and control animals. Our analysis revealed that after acquisition of fear conditioning 26 genes were regulated differently in the basolateral amygdala of both groups. Thus, our study provides the first evidence that not only the damage to the neuronal pathways but also altered composition or activity level of molecular machinery responsible for formation of emotional memories within surviving pathways can contribute to impairment in emotional learning in epileptogenic animals. Understanding the function of those genes in emotional learning provides an attractive avenue for identification of novel drug targets for treatment of emotional disorders after epileptogenesis-inducing insult. Experiment Overall Design: Experiment description: Experiment Overall Design: Array: Rat Genome 230-2.0 (Affymetrix). Experiment Overall Design: Samples: 2 biological replicates from 4 experimental groups (control unpaired = CU, CU1, control paired = CP, CP1, epileptogenic unpaired = EU, EU1, epileptogenic paired = EP, EP1). Experiment Overall Design: Animals&model: Amygdala stimulation model (Nissinen et al., 2000): Experiment Overall Design: control (C) animals = operated, not stimulated; Experiment Overall Design: epileptogenic (E) animals = stimulated, responded with "good" status epilepticus (at least 40HAFDs within first 3h of SE), not expressing spontaneous seizures through the whole study. Experiment Overall Design: All animals received 5 habituation session to the fear conditioning apparatus lasting 10 min, starting on day 5 (2 sessions on day 5 and 6 and 1 session on day 7) after stimulation (induction of SE). Experiment Overall Design: On 8th day after stimulation: Experiment Overall Design: unpaired (U) = twice received: 2min in apparatus â footshock (1.5mA, 1s)â tone (75dB for 20 sec) Experiment Overall Design: paired (P) = twice received: 2min in apparatus â tone (75dB for 20 sec) co-terminated by footshock (1.5mA, 1s). Experiment Overall Design: RNA isolation: decapitation â ipsilateral temporal lobe isolated, embed in OCT and frozen in -70C. Cut into 10µm sections, thionin stained (Ambion protocol), basal and lateral nuclei of the amygdala laser-microdissected; total cellular RNA isolated with PicoPure RNA isolation kit (Arcturus). Experiment Overall Design: RNA amplification: 30ng of of total cellular RNA from each rat underwent of 2 rounds of amplification using MessageAmp II aRNA kit (Ambion), according to manufacturer protocol (in vitro transcription time 14h in both rounds). Experiment Overall Design: Sample pooling: aRNA from 2 animals was pooled (10µg in total = 2x5µg) and 8 samples were labeled and hybridized: CP, CP1, CU, CU1, EP, EP1, EU, EU1; (altogether aRNA from 16 rats was used).
2009-02-26 | E-GEOD-13624 | biostudies-arrayexpress
Project description:We performed single-cell RNA-seq of full, microdissected and dissociated mouse amygdala, 2h, 8h or 24h after tone-cued fear conditioning (CFC), and 2h after recall (exposure to CS only, 24h post-CFC), and naive homecage controls.
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Project description:Using Illumina MouseWG-6v2 microarrays, we investigated the gene transcription changes in microglia and peripheral monocytes after contextual fear conditioning of C57BL/6J mice. Mice were trained with or without a single minimized footshock stimulation (0-s or 2-s, 0.4 mA) and re-exposed to the training context without footshock for three different durations 24 h later: 0 min (FS0), 3 min (FS3), or 30 min (FS30). Whole brain microglia and peripheral monocytes were prepared 24 h after re-exposure using a neural tissue dissociation kit, including non-footshock controls for two re-exposure durations (Con3 and Con30). The data can be valuable for researchers interested in glial cells and neurotransmission studies and are related to the research article “Contextual fear conditioning regulates synapse-related gene transcription in mouse microglia”.
2022-10-28 | E-MTAB-12361 | biostudies-arrayexpress
Project description:This dataset constitutes the first RNA-seq study of gene expression following contextual fear conditioning in the mouse hippocampus. 15 total samples were analyzed, including animals trained in a contexual conditioning paradigm (FC) and controls. Tissue was collected at 30 minutes (FC), as well as 30 minutes after testing for retrieval of the memory (RT). Testing was performed at 24 hours after training over a 5-minute interval. Animals that were handled but not trained were dissected at the same time of day to control for variations due to circadian rhythms (CC3). The protocol was repeated over the course of 5 days to obtain 9 animals (2 hippocampi) per group, so that 5 independent FC experiments were represented in each time point and all animals for each group were dissected at the exactly the same time of day.
2015-07-22 | E-GEOD-63412 | biostudies-arrayexpress
Project description:This experiment uses a transgenic mouse that allows for activity-induced expression of an HA-tagged ribosome in an inducible and cre-dependent manner. This allowed us to assess long-lasting gene-expression changes in neurons active during contextual fear conditioning. Previous studies have used similar systems to look a transient changes in gene expression in these neurons, but we developed a system to look at long lasting changes. The workflow includes tissue dissection of the prefrontal cortex, tissue homogenization followed by an immunoprecipitation of the tagged ribosomes using antibodies against HA. RNA bound to the ribosomes is then purified, a cDNA library is prepared and RNAseq was performed. The experimental group was fear conditioned and the control group was left in their homecage for induction of HA- expression in active neurons.
2020-03-27 | E-MTAB-7836 | biostudies-arrayexpress
Project description:miRNA profiling was carried out using the miRCURY LNA™ microRNA Array (6th gen - hsa, mmu & rno) miRNA were profiled in amygdala brain tissue obtained from adult mice 30 mins after auditory fear conditioning and expression levels compared to tissue obtained from Home cage controls Adult male mice were fear conditioned using tone-shock pairings and brains were harvested 30 mins later. The brains of Home Cage controls and Fear Conditioned animals (n = 4/group) were then punched to collect amygdala tissue. miRNA were extracted using the Qiagen miRNeasy Kit, and then shipped to Exiqon. Exiqon performed labeling, hybridization and data analysis after use of the miRCURY LNA™ microRNA Array (6th gen - hsa, mmu & rno). https://www.exiqon.com/ls/Documents/Scientific/miRCURY-LNA-microRNA-Array-6th-gen-hsa-mmu-rno-manual.pdf
2014-09-30 | E-GEOD-59072 | biostudies-arrayexpress
Project description:Mice with the two calcium-stmulated adenylyl cyclase isoforms (AC1 and AC8; DKO mice) knocked-out show conditioned fear memory deficits. We assessed gene expression changes at baseline and several time points after conditioned fear learning to assess transcriptional changes at different stages of learning. Transcriptional changes were assessed in the amydgdala and hippocampus of DKO and wild-type mice. Mice either received no treatment (baseline) or were subjected to conditioned fear training (one 0.7mA x 2 sec shock). Amygdala and hippocampal tissue from wild-type and DKO (AC1 and AC8 KO) mice was used. Samples were extracted at baseline (-5 min before conditioned fear training), 0 hr, 1 hr, or 48 hr after a 5 min conditioned fear training trial, or at 1 wk after a 5 min conditioned fear testing trial. RNA samples from 5-10 mice were pooled per array with one array per genotype/brain region/time point for a total of 20 arrays. mRNA was reverese transcribed, labeled and hybridized to Affymetric Mouse Gene ST 1.0 Arrays.
2010-10-19 | E-GEOD-23008 | biostudies-arrayexpress
Project description:There is a growing appreciation of the role of non-coding RNAs in the regulation of gene and protein expression. Long non-coding RNAs can modulate splicing by hybridizing with precursor messenger RNAs (pre-mRNAs) and influence RNA editing, mRNA stability, translation activation and microRNA-mRNA interactions by binding to mature mRNAs. LncRNAs are highly abundant in the brain and have been implicated in neurodevelopmental disorders. Long intergenic non-coding RNAs are the largest subclass of lncRNAs and play a crucial role in gene regulation. We used RNA sequencing and bioinformatic analyses to identify lincRNAs and their predicted mRNA targets associated with fear extinction that was induced by intra-hippocampally administered D-cycloserine in an animal model investigating the core phenotypes of PTSD. We identified 43 differentially expressed fear extinction related lincRNAs and 190 differentially expressed fear extinction related mRNAs. Eight of these lincRNAs were predicted to interact with and regulate 108 of these mRNAs and seven lincRNAs were predicted to interact with 22 of their pre-mRNA transcripts. On the basis of the functions of their target RNAs, we inferred that these lincRNAs bind to nucleotides, ribonucleotides and proteins and subsequently influence nervous system development, and morphology, immune system functioning, and are associated with nervous system and mental health disorders. Quantitative trait loci that overlapped with fear extinction related lincRNAs, included serum corticosterone level, neuroinflammation, anxiety, stress and despair related responses. This is the first study to identify lincRNAs and their RNA targets with a putative role in transcriptional regulation during fear extinction.
2020-03-01 | E-MTAB-8647 | biostudies-arrayexpress
Project description:Extinction learning refers to the phenomenon that a previously learned response to an environmental stimulus, for example the expression of an aversive behavior upon exposure to a specific context, is reduced when the stimulus is repeatedly presented in the absence of a previously paired aversive event. Extinction of fear memories has been implicated with the treatment of anxiety disease but the molecular processes that underlie fear extinctionare only beginning to emerge. Here we show that fear extinction initiates up-regulation of hippocampal insulin-growth factor 2 (Igf2) and down-regulation of insulin-growth factor binding protein 7 (Igfbp7). In line with this observation we demonstrate that IGF2 facilitates fear extinction, while IGFBP7 impairs fear extinction in an IGF2-dependent manner. Furthermore, we identify one cellular substrate of altered IGF2-signaling during fear extinction. To this end we show that fear extinction-induced IGF2/IGFBP7-signaling promotes the survival of 17-19 day-old newborn hippocampal neurons. In conclusion, our data suggests that therapeutic strategies that enhance IGF2-signaling and adult neurogenesis might be suitable to treat disease linked to excessive fear memory. We employed mice to investigate fear extinction in the hippocampus-dependent contextual fear conditioning paradigm. To this end, male C57BL/6J mice were exposed to the fear conditioning box (context) followed by an electric foot-shock which elicits the acquisition of conditioned contextual fear. For extinction training animals were repeatedly reexposed to the conditioned context on consecutive days (24h interval) without receiving the footshockagain (extinction trial, E). This procedure eventually results in the decline of the aversive freezing behavior. Mice that were exposed to the conditioning context without receiving fear conditioning training served as control groups. To gain a better understanding of the molecular processes underlying fear extinction we performed a genome-wide analysis of the hippocampal transcriptome during fear extinction. In the employed paradigm fear extinction is a gradual process. To capture the longitudinal course of fear extinction we decided to perform hippocampal microarray analysis at two time points: (1) After the first extinction trial (E1) when animals display high levels of aversive freezing behavior and (2) at the extinction trial on which the freezing behavior was significantly reduced when compared to E1. This extinction trial, in the case of this experiment E5, we termed “extinction trial low freezing” (ELF). Mice that were exposed to the conditioning context without receiving fear conditioning training served as control groups (3). For all three groups we hybridized 5 samples (biological replicates).
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