RNA-seq of cortical brain from Grin1-exon5 constitutive vs. Grin1-exon5 knockout mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE136983 | GEO | 2019/10/31
REPOSITORIES: GEO
Similar Datasets
Project description:RNA-seq of cortical brain from Grin1-exon5 constitutive vs. Grin1-exon5 knockout mice
| PRJNA564150 | ENA
Project description:Among all voltage-gated calcium channels, the T-type Ca2+ channels encoded by the Cav3 genes are highly expressed in the hippocampus, which is associated with contextual, temporal and spatial learning and memory. However, the specific involvement of the Cav3.2 T-type Ca2+ channel in these hippocampus-dependent types of learning and memory remains unclear. To investigate the functional role of the 1H channel in learning and memory, we subjected Cav3.2 homozygous, heterozygous knockout and their wild-type littermates to hippocampus-dependent behavioral tasks, including trace fear conditioning (TFC), the Morris water-maze and passive avoidance. The Cav3.2-/- mice performed normally in the Morris water-maze and auditory trace fear conditioning tasks but were impaired in the context-cued trace fear conditioning, step-down and step-through passive avoidance tasks. Furthermore, long-term potentiation (LTP) could be induced for 180 minutes in hippocampal slices of WTs and Cav3.2+/- mice, whereas LTP persisted for only 120 minutes in Cav3.2-/- mice. To determine whether the hippocampal formation is responsible for the impaired behavioral phenotypes , we next performed experiments locally knock down function of the Cav3.2 T-type Ca2+ channel in the hippocampus. Wild-type mice infused with mibefradil exhibited similar behaviors as homozygous knockouts. Finally, microarray analyses indicated that Cav3.2-/- and WT mice presented distinct hippocampal transcriptome profiles. Taken together, our results demonstrate that retrieval of context-associated memory is dependent on the Cav3.2 T-type Ca2+ channel. After WT and Cav3.2 KO mice retrieval of context-associated memory, three right hippocampi of each group were dissected, pooled together and homogenized. The products of experimental and naive groups were used to acquire expression profiles of a total of 29,922 unique genes. Two replicates per group.
2013-02-28 | E-GEOD-30845 | biostudies-arrayexpress
Project description:Among all voltage-gated calcium channels, the T-type Ca2+ channels encoded by the Cav3 genes are highly expressed in the hippocampus, which is associated with contextual, temporal and spatial learning and memory. However, the specific involvement of the Cav3.2 T-type Ca2+ channel in these hippocampus-dependent types of learning and memory remains unclear. To investigate the functional role of the 1H channel in learning and memory, we subjected Cav3.2 homozygous, heterozygous knockout and their wild-type littermates to hippocampus-dependent behavioral tasks, including trace fear conditioning (TFC), the Morris water-maze and passive avoidance. The Cav3.2-/- mice performed normally in the Morris water-maze and auditory trace fear conditioning tasks but were impaired in the context-cued trace fear conditioning, step-down and step-through passive avoidance tasks. Furthermore, long-term potentiation (LTP) could be induced for 180 minutes in hippocampal slices of WTs and Cav3.2+/- mice, whereas LTP persisted for only 120 minutes in Cav3.2-/- mice. To determine whether the hippocampal formation is responsible for the impaired behavioral phenotypes , we next performed experiments locally knock down function of the Cav3.2 T-type Ca2+ channel in the hippocampus. Wild-type mice infused with mibefradil exhibited similar behaviors as homozygous knockouts. Finally, microarray analyses indicated that Cav3.2-/- and WT mice presented distinct hippocampal transcriptome profiles. Taken together, our results demonstrate that retrieval of context-associated memory is dependent on the Cav3.2 T-type Ca2+ channel. After WT and Cav3.2 KO mice retrieval of context-associated memory, three left hippocampi of each group were dissected, pooled together and homogenized. The products of experimental and naive groups were used to acquire expression profiles of a total of 29,922 unique genes. Two replicates per group.
2013-02-28 | E-GEOD-30842 | biostudies-arrayexpress
Project description:Neurons utilize glucose to generate adenosine triphosphate (ATP) essential for their survival, excitability and synaptic signaling, as well as initiating changes in neuronal structure and function. Defects in oxidative metabolism and mitochondria functions are also associated with aging and diverse human neurological diseases1-4. While neurons are known to adapt their metabolism to meet the increased energy demands of complex behaviors such as learning and memory, the molecular underpinnings regulating this process remain poorly understood4-6. Here we show that the orphan nuclear receptor estrogen related receptor gamma (ERRγ) becomes highly expressed during retinoic-acid induced neurogenesis and is widely expressed in neuronal nuclei throughout the brain. Mechanistically, we show that ERRγ directly orchestrates the expression of networks of genes involved in mitochondrial oxidative phosphorylation and energy generation in neurons. The importance of this regulation is evidenced by decreased adaptive metabolic capacity in cultured neurons lacking ERRγ, and reduced long-term potentiation (LTP) in ERRγ-/- hippocampal slices. Notably, the defect in LTP was rescued by the metabolic intermediate pyruvate, functionally linking the ERRγ knockout metabolic phenotype and memory formation. Consistent with this notion, mice lacking neuronal ERRγ exhibit defects in spatial learning and memory. These findings implicate ERRγ in the metabolic adaptations required for long-term memory formation. We used microarray analysis to compare the genome-wide gene expression changes between wild type (WT) and ERRγ-/- P0 cerebral cortex as it contains mainly neuronal lineage at this stage compared to adult cortex.
2015-09-03 | E-GEOD-47133 | biostudies-arrayexpress
Project description:Long-term potentiation (LTP) of synaptic transmission is recognized as a cellular mechanism for learning and memory storage. Although de novo gene transcription is known to be required in the formation of stable LTP, the molecular mechanisms underlying synaptic plasticity remain elusive.This study investigates the DNA-methylation levels of promoters and CpG-islands of LTP-associated genes identified from Maag et al. 2015 (DOI: 10.3389/fnins.2015.00351) (See E-MTAB-3375).
2017-03-16 | E-MTAB-4919 | biostudies-arrayexpress
Project description:Among all voltage-gated calcium channels, the T-type Ca2+ channels encoded by the Cav3 genes are highly expressed in the hippocampus, which is associated with contextual, temporal and spatial learning and memory. However, the specific involvement of the Cav3.2 T-type Ca2+ channel in these hippocampus-dependent types of learning and memory remains unclear. To investigate the functional role of the 1H channel in learning and memory, we subjected Cav3.2 homozygous, heterozygous knockout and their wild-type littermates to hippocampus-dependent behavioral tasks, including trace fear conditioning (TFC), the Morris water-maze and passive avoidance. The Cav3.2-/- mice performed normally in the Morris water-maze and auditory trace fear conditioning tasks but were impaired in the context-cued trace fear conditioning, step-down and step-through passive avoidance tasks. Furthermore, long-term potentiation (LTP) could be induced for 180 minutes in hippocampal slices of WTs and Cav3.2+/- mice, whereas LTP persisted for only 120 minutes in Cav3.2-/- mice. To determine whether the hippocampal formation is responsible for the impaired behavioral phenotypes , we next performed experiments locally knock down function of the Cav3.2 T-type Ca2+ channel in the hippocampus. Wild-type mice infused with mibefradil exhibited similar behaviors as homozygous knockouts. Finally, microarray analyses indicated that Cav3.2-/- and WT mice presented distinct hippocampal transcriptome profiles. Taken together, our results demonstrate that retrieval of context-associated memory is dependent on the Cav3.2 T-type Ca2+ channel.
2013-02-28 | GSE30845 | GEO
Project description:Among all voltage-gated calcium channels, the T-type Ca2+ channels encoded by the Cav3 genes are highly expressed in the hippocampus, which is associated with contextual, temporal and spatial learning and memory. However, the specific involvement of the Cav3.2 T-type Ca2+ channel in these hippocampus-dependent types of learning and memory remains unclear. To investigate the functional role of the 1H channel in learning and memory, we subjected Cav3.2 homozygous, heterozygous knockout and their wild-type littermates to hippocampus-dependent behavioral tasks, including trace fear conditioning (TFC), the Morris water-maze and passive avoidance. The Cav3.2-/- mice performed normally in the Morris water-maze and auditory trace fear conditioning tasks but were impaired in the context-cued trace fear conditioning, step-down and step-through passive avoidance tasks. Furthermore, long-term potentiation (LTP) could be induced for 180 minutes in hippocampal slices of WTs and Cav3.2+/- mice, whereas LTP persisted for only 120 minutes in Cav3.2-/- mice. To determine whether the hippocampal formation is responsible for the impaired behavioral phenotypes , we next performed experiments locally knock down function of the Cav3.2 T-type Ca2+ channel in the hippocampus. Wild-type mice infused with mibefradil exhibited similar behaviors as homozygous knockouts. Finally, microarray analyses indicated that Cav3.2-/- and WT mice presented distinct hippocampal transcriptome profiles. Taken together, our results demonstrate that retrieval of context-associated memory is dependent on the Cav3.2 T-type Ca2+ channel.
2013-02-28 | GSE30842 | GEO
Project description:Neurons utilize glucose to generate adenosine triphosphate (ATP) essential for their survival, excitability and synaptic signaling, as well as initiating changes in neuronal structure and function. Defects in oxidative metabolism and mitochondria functions are also associated with aging and diverse human neurological diseases1-4. While neurons are known to adapt their metabolism to meet the increased energy demands of complex behaviors such as learning and memory, the molecular underpinnings regulating this process remain poorly understood4-6. Here we show that the orphan nuclear receptor estrogen related receptor gamma (ERRγ) becomes highly expressed during retinoic-acid induced neurogenesis and is widely expressed in neuronal nuclei throughout the brain. Mechanistically, we show that ERRγ directly orchestrates the expression of networks of genes involved in mitochondrial oxidative phosphorylation and energy generation in neurons. The importance of this regulation is evidenced by decreased adaptive metabolic capacity in cultured neurons lacking ERRγ, and reduced long-term potentiation (LTP) in ERRγ-/- hippocampal slices. Notably, the defect in LTP was rescued by the metabolic intermediate pyruvate, functionally linking the ERRγ knockout metabolic phenotype and memory formation. Consistent with this notion, mice lacking neuronal ERRγ exhibit defects in spatial learning and memory. These findings implicate ERRγ in the metabolic adaptations required for long-term memory formation. We used ChIP-Seq analysis to determine the genome-wide binding of ERRγ in neurons derived from ES cells.
2015-09-03 | E-GEOD-47134 | biostudies-arrayexpress
Project description:We performed an RNA Sequencing experiment on dorsal hippocampal tissue from four groups of animals: Baf53b+/- homecage (Baf53b+/- HC); Baf53b+/- behavior (Baf53b+/- Beh); wildtype homecage (WT HC); and wildtype behavior (WT Beh). Homecage animals were sacrificed directly from the animal's cage. Behavior animals were sacrificed thirty minutes following Object Location Memory training. The objective of this study was to examine activity regulated gene expression following a learning event (HC vs Beh) in wildtype and Baf53b+/- mutant mice. Examination of gene expression following a learning event in wildtype and Baf53b+/- mutant mice in dorsal hippocampus.
2013-03-24 | E-GEOD-44229 | biostudies-arrayexpress
Project description:The conventional notion of “immune privilege” of the brain has been revised to accommodate its infiltration, at steady state, by immune cells that participate in normal neurophysiology (Louveau, Trends Immunol 2015; Kipnis science 2016; Filiano, Nat Rev Neurosciences 2017). Surprisingly, such neuroimmune functions have been linked to “pro-inflammatory” cytokines like IL-4 or IFN-α, shown to control behavioural and social cognition (Derecki, JEM 2010; Filiano, Nature 2016). Here we identify a pro-cognitive role for IL-17 in short-term memory that derives from a previously unknown meningeal-resident γδ T cell subset. This was mostly composed of foetal thymic-derived Vγ6+ T cells, found in the meninges at birth and persisting throughout life, where they were strikingly polarized towards IL-17 production. In fact, γδ T cells were the overwhelming source of meningeal IL-17, whereas IFN-γ was mostly provided by T cells. To assess whether the constitutive production of IL-17 by γδ T cells influenced the cognitive performance of mice, we tested TCRδ-/-, IL-17-/- and respective WT littermate control mice in classical learning paradigms. We observed that mice deficient either for γδ T cells or IL-17 displayed impaired short-term memory in the Y maze paradigm, while retaining normal long-term spatial memory in the Morris water maze. A detailed proteomics analysis of the hippocampus provided mechanistic insight into reduced plasticity of the glutamatergic synapses in the absence of IL-17, which associated with impaired Long Term Potentiation (LTP). Conversely, IL-17 enhanced glial cell production of Brain Derived Neurotropic Factor (BDNF), whose exogenous provision rescued the LTP defect of IL-17-/- animals. Altogether, our data demonstrate that foetal-derived γδ T cells populate the brain meninges where they regulate synaptic plasticity and short-term memory through a non-inflammatory IL-17-dependent mechanism.
2019-10-16 | PXD007574 | Pride