Cell types in the mouse amygdala and their transcriptional response to fear conditioning
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Illumina NovaSeq 6000
ORGANISM(S): Mus musculus
SUBMITTER: Amit Zeisel
PROVIDER: E-MTAB-12096 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Anterior interpositus nucleus (AIN) is a proposed site of memory formation of eyeblink conditioning. A large part of the underlying molecular events, however, remains unknown. To elucidate molecular mechanisms, we examined transcriptional changes in the AIN of mice trained with delayed-type eyeblink conditioning Experiment Overall Design: 7-d paired training group: Mice received a surgery for implanting four Teflon-coated stainless-steel wires in their left eyelid and a headstage on their head. After 3daysâ?? recovery, they were trained with paired paradigm of conditioned stimulus (CS) and unconditioned stimulus (US) for 7 days: A 352-ms tone CS (1kHz, 83~85dB) was delivered first and a 100ms periorbital shock US (100kHz square pluses) were delivered with 252ms after the onset of CS, and they co-terminated. In case of 7-d unpaired training group, A CS and a US were delivered in an explicitly unpaired, pseudorandomized manner for 7 days. After the last trial was given, anterior interpositus was immediately sampled in 10 to 30 min from the sacrifice.
2008-06-12 | E-GEOD-3652 | biostudies-arrayexpress
Project description:This SuperSeries comprises the following subset Series:; GSE3651: The AIN-centered DCN of delayed-type eyeblink conditioned mice: 3-d paired training and sham negative control groups; GSE3652: The AIN-centered DCN of delayed-type eyeblink conditioned mice: 7-d paired and 7-d unpaired training groups; Anterior interpositus nucleus (AIN) is a proposed site of memory formation of eyeblink conditioning. A large part of the underlying molecular events, however, remains unknown. To elucidate molecular mechanisms, we examined transcriptional changes in the AIN of mice trained with delayed-type eyeblink conditioning; The data are not directly comparable between GSE3651 and GSE3652, given the different experimental time periods and amounts of cRNA used for hybridizations. Experiment Overall Design: Refer to individual Series
2008-06-12 | E-GEOD-3713 | biostudies-arrayexpress
Project description:Anterior interpositus nucleus (AIN) is a proposed site of memory formation of eyeblink conditioning. A large part of the underlying molecular events, however, remains unknown. To elucidate molecular mechanisms, we examined transcriptional changes in the AIN of mice trained with delayed-type eyeblink conditioning Experiment Overall Design: 3-d paired training group: Mice received a surgery for implanting four Teflon-coated stainless-steel wires in their left eyelid and a headstage on their head. After 3daysâ?? recovery, they were trained with paired paradigm of conditioned stimulus (CS) and unconditioned stimulus (US) for 3days: A 352-ms tone CS (1kHz, 83~85dB) was delivered first and a 100ms periorbital shock US (100kHz square pluses) were delivered with 252ms after the onset of CS, and they co-terminated. After the last trial was given, anterior interpositus was immediately sampled in 10 to 30 min from the sacrifice. Experiment Overall Design: Sham negative control group: Mice received a surgery for implanting four Teflon-coated stainless-steel wires in their left eyelid and a headstage on their head. After recovery, anterior interpositus nucleus-centered deep cerebellar nuclei were immediately sampled in 10 to 30 min from the sacrifice. Experiment Overall Design: ~10-15 anterior interpositus-centered deep cerebellar nuclei ipsilateral to the eye implanted with four wires were pooled into the same sham control or training group and subjected to microarray analysis.
2008-06-12 | E-GEOD-3651 | biostudies-arrayexpress
Project description:Understanding the mechanisms by which long-term memories are formed and stored in the brain represents a central aim of neuroscience. Prevailing theory suggests that long-term memory encoding involves early plasticity within hippocampal circuits, while reorganization of the neocortex is thought to occur weeks to months later to subserve remote memory storage. Here we report that long-term memory encoding can elicit early transcriptional, structural and functional remodeling of the neocortex. Parallel studies using genome-wide RNA-sequencing, ultrastructural imaging, and whole-cell recording in wild-type mice suggest that contextual fear conditioning initiates a transcriptional program in the medial prefrontal cortex (mPFC) that is accompanied by rapid expansion of the synaptic active zone and postsynaptic density, enhanced dendritic spine plasticity, and increased synaptic efficacy. To address the real-time contribution of the mPFC to long-term memory encoding, we performed temporally precise optogenetic inhibition of excitatory mPFC neurons during contextual fear conditioning. Using this approach, we found that real-time inhibition of the mPFC inhibited activation of the entorhinal-hippocampal circuit and impaired the formation of long-term associative memory. These findings suggest that encoding of long-term episodic memory is associated with early remodeling of neocortical circuits, identify the prefrontal cortex as a critical regulator of encoding-induced hippocampal activation and long-term memory formation, and have important implications for understanding memory processing in healthy and diseased brain states. 4 biological replicates per group were analyzed. The material analyzed was medial prefrontal cortex (mPFC; anterior cingulate cortex subregion) from both brain hemispheres, from which total RNA was extracted.
2014-06-16 | E-GEOD-58510 | 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:Learning and memory processes are accompanied by rearrangements of synaptic protein networks. While various studies have demonstrated the regulation of individual synaptic proteins during these processes, much less is known about the complex regulation of entire synaptic proteomes. Recently, we reported that auditory discrimination learning in mice is associated with a relative down-regulation of proteins involved in the structural organization of synapses in various brain regions. Aiming at the identification of biological processes and signaling pathways involved in auditory memory formation, here a label-free quantification approach was utilized to identify regulated synaptic junctional proteins and phosphoproteins in the auditory cortex, frontal cortex, hippocampus and striatum of mice 24 h after the learning experiment. Twenty proteins, including postsynaptic scaffolds, actin modeling proteins and RNA-binding proteins, were regulated in at least three brain regions pointing to common, cross-regional mechanisms. Most of the detected synaptic proteome changes were, however, restricted to individual brain regions. For example, several members of the Septin family of cytoskeletal proteins were upregulated only in the hippocampus, while Septin-9 was down-regulated in the hippocampus, the frontal cortex and the striatum. Meta analyses utilizing several databases were employed to identify underlying cellular functions and biological pathways.
2016-04-14 | PXD003089 | Pride
Project description:The mechanisms underlying age-associated memory impairment are not well understood. We have shown that the onset of memory disturbances in the aging brain is associated with altered hippocampal chromatin plasticity. During learning, aged mice display a specific deregulation of histone H4 lysine 12 (H4K12) acetylation. To analyze if deregulated H4K12 acetylation impacts on learning-induced gene-expression required for memory consolidation we performed a high-density oligonucleotide microarray to compare the entire hippocampal gene-expression profile of 3 and 16-month-old mice during memory consolidation. In order to identify genes differentially regulated between 3- and 16-month old mice upon fear conditioning we subjected 3- and 16-month old mice to fear conditioning (4 mice each group, total 8 mice) . Mice of the same age that were handled but not subjected to any of the employed behavior paradigms served as control (4 mice 3-month old and 4 mice 16-month old, total 8 mice). During fear conditioning mice are subjected to a novel context followed by a mild electric foot-shock (context-shock exposure). In order to identify genes that are differentially regulated upon fear conditioning and are specific to associative learning we also tested the hippocampal gene-expression profile of 3-month old mice subjected to the same context-exposure that is not followed by a foot-shock (Context-exposure) (4 mice) or receive an immediate foot shock once they are placed in the context and only afterwards are allowed to explore the context (shock-context exposure) (4 mice). In order to identify genes that are regulated upon fear conditioning and are specific to associative learning we compared the hippocampal gene-expression profile of mice subjected to fear conditioning (context-shock), context or shock-context exposure regarding to their age-matched control mice (3 month old) mentioned above (control). Hippocampi from each mice were tested resulting to 24 samples which were separately hybridized (OneColor Array Design).
2010-04-28 | E-GEOD-20270 | biostudies-arrayexpress
Project description:Staphylococcus aureus USA300 and Pseudomonas aeruginosa PAO1 were cultured in microaerobiosis (sealed bottles using a 1:4 medium-to-flask volume ratio without agitation) in Triptic Soy Broth (TSB; Oxoid) supplemented with 0.5% KNO3. S. aureus and P. aeruginosa monocultures were inoculated at a DO600 of 0.05 and incubated for 2h at 37°C. After that, cultures were split in two and furtherly incubated for 2h at 37°C (control) or 39°C (heat shock). A similar protocol was employed for co-culture experiments, where S. aureus and P. aeruginosa were co-inoculated each at a DO600 of 0.05 and followed the same protocol.
2024-01-18 | E-MTAB-12581 | biostudies-arrayexpress
Project description:The purpose of this study was to determine whether there were differences in gene expression in the hippocampus, a part of the brain involved in memory consolidation, between male mice with age-related memory deficits (SAMP8 mice) and control mice with no age-related memory deficits. The senescence-accelerated mouse (SAMP8) strain exhibits decreased learning and memory and increased amyloid beta peptide (Aβ) accumulation at 12 months compared to 4 months. To detect differences in gene expression in SAMP8 mice, we used a Control mouse that was a 50% cross between SAMP8 and CD-1 mice and which showed no memory deficits (50% SAMP8 mouse). We then compared gene expression in the hippocampus of 4 month and 12 month old SAMP8 and Control mice using Affymetrix gene arrays. At 12 months, but not at 4 months, pathway analysis revealed significant differences in the Long Term Potentiation (LTP) (6 genes), Phosphatidylinositol Signaling (6 genes), and Endocytosis (10 genes) pathways. The changes in LTP included MAPK signaling (N-ras, CREB binding protein, protein phosphatase inhibitor 1) and Ca-dependent signaling (PI receptors 1 and 2 and phospholipase C). Changes in phosphatidylinositol signaling genes suggested altered signaling through PI3-kinase, and Western blotting revealed phosphorylation changes in AKT and 70S6K. Changes in the Endocytosis pathway involved genes related to clathrin-mediated endocytosis (dynamin and clathrin). Endocytosis is required for receptor recycling, is involved in Aβ metabolism, and is regulated by phosphatidylinositol signaling. In summary, these studies demonstrate altered genes expression in three SAMP8 hippocampal pathways associated with memory formation and consolidation. These pathways may provide new therapeutic targets in addition to targeting Aβ metabolism itself. Global differential profiling of hippocampal gene expression (4 month and 12 month old SAMP8 and Control mice) was performed using Affymetrix GeneChip® Mouse Genome 430 2.0 Arrays. At 12 months, but not at 4 months, pathway analysis revealed significant differences in the Long Term Potentiation (LTP) (6 genes), Phosphatidylinositol Signaling (6 genes), and Endocytosis (10 genes) pathways. The changes in LTP included MAPK signaling (N-ras, CREB binding protein, protein phosphatase inhibitor 1) and Ca-dependent signaling (PI receptors 1 and 2 and phospholipase C). Changes in phosphatidylinositol signaling genes suggested altered signaling through PI3-kinase, and Western blotting revealed phosphorylation changes in AKT and 70S6K. Changes in the Endocytosis pathway involved genes related to clathrin-mediated endocytosis (dynamin and clathrin). Endocytosis is required for receptor recycling, is involved in Aβ metabolism, and is regulated by phosphatidylinositol signaling. In summary, these studies demonstrate altered genes expression in three SAMP8 hippocampal pathways associated with memory formation and consolidation. These pathways may provide new therapeutic targets in addition to targeting Aβ metabolism itself. 2-way ANOVA (2 x 2 conditions, n=4). First variable was age (4 and 12 months) and second variable was mouse strain (Control and SAMP8). This results in 4 groups: Control-4 month, Control-12 month, SAMP8-4 month, and SAMP8-12 month. Each group had 4 biological replicates (4 mice). The ”Control” mice were a 50% backcross of the SAMP8 mice with CD-1 mice (50% SAMP8 mice). These mice were closely related to SAMP8 mice but exhibited no memory deficits at 4 or 12 months. The SAMP8 mice had memory deficits at 12 months but not at 4 months.
2013-08-30 | E-GEOD-49699 | biostudies-arrayexpress
Project description:The purpose of this study was to determine the effect of peripheral (IV) administration of AβPP antisense on hippocampal gene expression as well as on learning and memory as measured by T-maze in adult male mice aged 12 months. The AβPP antisense treatment reversed learning and memory deficits and altered the expression of 944 hippocampal genes, which are involved in a coordinated set of signaling pathways. Expression and pathway findings were verified at the protein and functional (phosphorylation) levels. Global differential profiling of hippocampal gene expression (12 month old adult mice: Control, SAMP8, SAMP8 + Random antisense, SAMP8 + AβPP antisense) was performed using Affymetrix GeneChip® Mouse Genome 430 2.0 Arrays. The AβPP antisense reversed the memory deficits and altered expression of 944 hippocampal genes. Pathway analysis showed significant gene expression changes in 9 pathways. These include the MAPK signaling pathway (P = 0.0078) and the phosphatidylinositol signaling pathway (P = 0.043), which we have previously shown to be altered in SAMP8 mice. The changes in these pathways contributed to significant changes in the Neurotropin (P = 0.0083) and Insulin Signaling (P = 0.015) pathways, which are known to be important in learning and memory. Changes in these pathways were accompanied by phosphorylation changes in the downstream target proteins p70S6K, GSK3β, ERK, and CREB. These changes in hippocampal gene expression and protein phosphorylation may suggest specific new targets for antisense therapy aimed at improving memory. One-way ANOVA (4 conditions, n=4). Variables were treatment (AβPP antisense, Random antisense, no treatment) and mouse strain (Control and SAMP8). This results in 4 groups: (All 12-month-old adult male mice) NT-Control, NT_SAMP8, Random_AS-SAMP8, and AβPP_AS-SAMP8. Each group had 4 biological replicates (4 mice). The 'Control' mice were a 50% backcross of the SAMP8 mice with CD-1 mice (50% SAMP8 mice). These mice were closely related to SAMP8 mice but exhibited no memory deficits at 4 or 12 months. The SAMP8 mice had memory deficits at 12 months but not at 4 months.
2015-02-13 | E-GEOD-65877 | biostudies-arrayexpress