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.
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2014-06-16 | E-GEOD-58510 | biostudies-arrayexpress
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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.
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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).
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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
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