Differential expression: associative and nonassociative learning
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE3963 | GEO | 2006/03/20
SECONDARY ACCESSION(S): PRJNA94221
REPOSITORIES: GEO
Similar Datasets
Project description:Hippocampus and amygdala expression was examined in naive, conditioned stimulus exposed, and fear conditioned mice 30 minutes after behavioral manipulation
2007-12-15 | E-GEOD-3963 | biostudies-arrayexpress
Project description:Fear extinction is an adaptive behavioral process critical for organism’s survival, but deficiency in extinction may lead to PTSD. While the amygdala and its neural circuits are critical for fear extinction, the molecular identity and organizational logic of cell types that lie at the core of these circuits remain unclear. Here we report that mice deficient for amygdala-enriched gastrin-releasing peptide gene (Grp-/-) exhibit enhanced neuronal activity in the basolateral amygdala (BLA) and stronger fear conditioning, as well as deficient extinction in stress-enhanced fear learning (SEFL). rAAV2-retro-based tracing combined with visualization of the GFP knocked in the Grp gene showed that BLA receives several GRPergic conditioned stimulus projections: from the indirect auditory thalamus-to-auditory cortex pathway, medial prefrontal cortex, ventral hippocampus and ventral tegmental area. Transcription of dopamine-related genes was decreased in BLA of Grp-/- mice following SEFL extinction recall, suggesting that the GRP may mediate fear extinction regulation by dopamine.
2021-12-01 | GSE164226 | GEO
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).
2011-08-07 | E-GEOD-31063 | biostudies-arrayexpress
Project description:The suppression of fear memory in the absence of danger (fear extinction) requires coordinated neural activity within the amygdala and medial prefrontal (prelimbic and infralimbic) cortex. Any behavior has a transcriptomic signature that is modified by environmental experiences, and specific genes are involved in functional plasticity and synaptic wiring during fear memory and extinction. In the present study, we investigated the effects of optogenetic manipulations of prelimbic pyramidal neurons on amygdala gene expression to analyze the specific transcriptional pathways involved in fear extinction. To this aim, transgenic mice (Thy1-COP4) having cortical and amygdala pyramidal neurons optogenetically excitable were (or not) fear-conditioned. During the extinction phase, the mice received optogenetic (or sham) stimulations to maintain the activation of the prelimbic pyramidal neurons and impair fear extinction. At the end of behavioral testing, electrophysiological (Excitatory Post-Synaptic Currents) and morphological (spinogenesis) correlates were evaluated in the pyramidal neurons of prelimbic cortex. Furthermore, transcriptomic cell-specific RNA-analyses (differential gene expression profiling and functional enrichment analyses) were performed in amygdala pyramidal neurons. Results demonstrate that pyramidal neurons of prelimbic cortex are involved in modulation of the fear responses during extinction phase and their optogenetic stimulation in fear-conditioned mice results in strong modifications of the amygdala transcriptome. Understanding the transcriptomic architecture of fear extinction may facilitate the comprehension of fear-related disorders.
2021-01-14 | GSE162417 | GEO
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.
2011-08-08 | GSE31063 | GEO
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: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:These data are from the brains (amygdala and hippocampus) of mice originally derived from a cross between C57BL/6J and A/J inbred strains. We used short-term selection to produce outbred mouse lines with differences in contextual fear conditioning, which is a measure of fear learning. We selected for a total of 4 generations. Fear learning differed in the selected lines and this difference was stronger with each successive generation of selection. We identified several QTLs for the selection response, including a highly significant QTL at the tyr locus (p < 9.6(-10)). We used Affymetrix microarrays to identify many differentially expressed genes in the amygdala and hippocampus of mice from the final generation of selection. Amygdala and hippocampus samples were rapidly dissected out of experimentally naïve mice from each selected line. Three samples were pooled and hybridized to each array. Experimentally naïve mice were used because the behavior of the mice can be reliably a nticipated due to their lineage. Thus these gene expression differences are not due to the response to human handling, foot shock or fear-inducing conditioned stimuli. We have a second similar study that focuses on a different selected population that was based on C57BL/6J and DBA/2J mice (see GES4035).
2006-01-13 | GSE4034 | GEO
Project description:These data are from the brains (amygdala and hippocampus) of mice originally derived from a cross between C57BL/6J and DBA/2J inbred strains. We used short-term selection to produce outbred mouse lines with differences in contextual fear conditioning, which is a measure of fear learning. We selected for a total of 4 generations. Fear learning differed in the selected lines and this difference was stronger with each successive generation of selection. These mice also showed differences for measures of anxiety-like behavior, but were not different for tests of non-fear motivated learning, suggesting that selection altered alleles that are specifically involved in emotional behaviors. We identified several QTLs for the selection response. We used Affymetrix microarrays to identify differentially expressed genes in the amygdala and hippocampus of mice from the final generation of selection. Amygdala and hippocampus samples were rapidly dissected out of experimentally naïve mice f rom each selected line. Three samples were pooled and hybridized to each array. Experimentally naïve mice were used because the behavior of the mice can be reliably anticipated due to their lineage. Thus, these gene expression differences are not due to the response to human handling, foot shock or fear-inducing conditioned stimuli. We have a second similar study that focuses on a different selected population that was based on C57BL/6J and A/J mice (see GES4034).
2006-01-13 | GSE4035 | GEO
Project description:Npas4 CUT&Tag dataset, Adult male WT C57BL/6J mice underwent discriminative fear conditioning and immediately injected saline. 90 minutes after fear conditioning, The amygdala tissue was extracted for further experiment. Npas4 CUT&Tag was performed to elucidate possible downstream targets which contributes regulation of fear expression during fear retreival.
2023-07-05 | GSE194069 | GEO