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Expression data from outer molecular of mouse hippocampus after entorhinal lesion

ABSTRACT: After lesion of the entorhinal cortex, expression changes occur in the denervated dentate gyrus. We used microarrays to examine gene expression changes underlying reorganization processes and identified down and upregulated genes during different time points after lesion

ORGANISM(S): Mus musculus

PROVIDER: GSE284334 | GEO | 2026/06/10

REPOSITORIES: GEO

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Expression data from granule cell layer of mouse hippocampus after entorhinal lesion

Project description:After lesion of the entorhinal cortex, expression changes occur in the denervated dentate gyrus. We used microarrays to examine gene expression changes underlying reorganization processes and identified down and upregulated genes during different time points after lesion

2026-06-10 | GSE284333 | GEO

Denervated mouse CA1 pyramidal neurons express homeostatic synaptic plasticity following entorhinal cortex lesion

Project description:Structural, functional, and molecular reorganization of denervated neural networks is often observed in neurological conditions. The loss of input is accompanied by homeostatic synaptic adaptations, which can affect the reorganization of denervated networks. However, a major challenge of denervation-induced homeostatic plasticity operating in complex neural networks is the specialization of neuronal inputs. Therefore, it remains unclear whether neurons respond similarly to the loss of distinct inputs. Here, we used in vitro entorhinal cortex lesion (ECL) and Schaffer collateral lesion (SCL) in mouse organotypic entorhino-hippocampal tissue cultures of either sex, and studied denervation-induced plasticity of CA1 pyramidal neurons. We observed accumulation of microglia, degeneration of presynaptic buttons and a reduction in dendritic spine numbers in the denervated layers three days after SCL and ECL, respectively. Transcriptome analysis of the CA1 region showed complex changes in differential gene expression following SCL and ECL compared to non-lesioned controls. An enrichment of differentially expressed synapse-related genes was observed specifically after ECL. Consistent with this finding, denervation-induced homeostatic plasticity of excitatory synapses was observed three days after ECL but not after SCL. Chemogenetic silencing of the EC but not CA3 confirmed the pathway-specific induction of homeostatic synaptic plasticity in CA1. Moreover, increased RNA oxidation was observed after SCL and ECL. These results reveal important commonalities and differences of distinct pathway lesions, and demonstrate a pathway-specific induction of denervation-induced homeostatic synaptic plasticity.

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Expression data from outer molecular of mouse hippocampus after entorhinal lesion

Project description:Expression data from outer molecular of mouse hippocampus after entorhinal lesion

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Denervated mouse CA1 pyramidal neurons express homeostatic synaptic plasticity following entorhinal cortex lesion

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Expression data from granule cell layer of mouse hippocampus after entorhinal lesion

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Molecular profiles of cognitive aging

Project description:Gene expression was measured from the dentate gyrus and entorhinal cortex harvested from human postmortem samples. We harvested the dentate gyrus DG from healthy human brains ranging from 33 to 88 years of age. Additionally, from each brain we harvested the entorhinal cortex (EC) as a within-brain control. Using Affymetrix microarray chips we generated gene-expression profiles of each individual tissue samples. DG expression levels were first normalized against the EC, and the normalized DG transcripts were then correlated against age.

2013-04-19 | E-GEOD-46193 | biostudies-arrayexpress

Molecular profiles of cognitive aging

Project description:Gene expression was measured from the dentate gyrus and entorhinal cortex harvested from human postmortem samples.

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Synaptopodin regulates denervation-induced plasticity at hippocampal mossy fiber synapses

Project description:Neurological diseases can lead to the denervation of brain regions caused by demyelination, traumatic injury or cell death. Nevertheless, the molecular and structural mechanisms underlying lesion-induced reorganization of denervated brain regions are a matter of ongoing investigation. In order to address this issue, we performed an entorhinal cortex lesion (ECL) in mouse organotypic entorhino-hippocampal tissue cultures of both sexes and studied denervation-induced plasticity of mossy fiber synapses, which connect dentate granule cells (dGCs) with CA3 pyramidal cells (CA3-PCs) and play important roles in spatial learning. Partial denervation caused a strengthening of excitatory neurotransmission in dGCs, in CA3-PCs, and their direct synaptic connections as revealed by paired recordings (GC-to-CA3). These functional changes were accompanied by ultrastructural reorganization of mossy fiber synapses, which regularly contain the plasticity-related protein synaptopodin and the spine apparatus organelle. We demonstrate that the spine apparatus organelle and its integral protein synaptopodin are associated with ribosomes in close proximity to synaptic sites and unravel a synaptopodin-related transcriptome. Notably, synaptopodin-deficient tissue preparations that lack the spine apparatus organelle, failed to express lesion-induced synaptic adjustments. Hence, synaptopodin and the spine apparatus organelle play a crucial role in regulating lesion-induced synaptic plasticity at hippocampal mossy fiber synapses.

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Transcription profiling of rat young and aged entorhinal cortex and hippocampus one month after entorhinal administration of BDNF lentivirus

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Pattern separation memory requires Cerebellin 4-Neogenin 1 signaling at dentate gyrus synapses

Project description:The ability to avoid confusion between similar episodic memories enables organismal survival and fitness. This evolutionarily conserved differentiation process of memories as distinct representations is known as pattern separation. A central role for the entorhinal cortex->dentate gyrus (EC->DG) circuit in pattern separation is well established, but the molecular mechanisms that enable this circuit to mediate pattern separation memory is not known. Here we show the involvement in murine pattern separation memory of a unique transsynaptic protein complex formed by Cerebellin-4, Neogenin-1, and neurexins that is known to be selectively required for long-term plasticity in the EC->DG circuit. In vivo deletion of either presynaptic Cerebellin-4 in the entorhinal cortex or of postsynaptic Neogenin-1 in the dentate gyrus impairs acquisition of pattern separation memory. Thus, we describe a specific memory function for a defined molecular complex at an identified synapse, providing direct support for the hypothesis that synaptic plasticity contributes to the encoding of memory.

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