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Cortical wiring by synapse type-specific control of local protein synthesis

ABSTRACT: Cortical wiring by synapse type-specific control of local protein synthesis

PROVIDER: PRJNA884646 | ENA |

REPOSITORIES: ENA

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Cortical wiring by synapse type-specific control of local protein synthesis

Project description:Neurons use local protein synthesis to support their morphological complexity, which requires independent control across multiple subcellular compartments up to the level of individual synapses. Here we identify a signaling pathway that regulates the local synthesis of proteins required to form excitatory synapses on parvalbumin-expressing (PV+) interneurons in the mouse cerebral cortex. This process involves regulation of the TSC subunit 2 (Tsc2) by the Erb-B2 receptor tyrosine kinase 4 (ErbB4), which enables local control of mRNA translation in a cell type-specific and synapse type-specific manner. Ribosome-associated mRNA profiling reveals a molecular program of synaptic proteins downstream of ErbB4 signaling required to form excitatory inputs on PV+ interneurons. Thus, specific connections use local protein synthesis to control synapse formation in the nervous system.

2022-11-24 | GSE214258 | GEO

Local calcium accumulations promote phagocyte-mediated synapse removal in cortical neuroinflammation

Project description:Cortical pathology contributes to chronic cognitive impairment of patients suffering from the neuroinflammatory disease multiple sclerosis (MS). How such gray matter inflammation affects neuronal structure and function is not well understood. Here we use functional and structural in vivo imaging in a mouse model of cortical MS to demonstrate that bouts of cortical inflammation disrupt cortical circuit activity coincident with a widespread, but transient loss of dendritic spines. Spines destined for removal show local calcium accumulations and are subsequently removed by invading macrophages or activated microglia. Targeting phagocyte activation with a new antagonist of the colony-stimulating factor 1 receptor prevents cortical synapse loss. Overall, our study identifies synapse loss as a key pathological feature of inflammatory gray matter lesions that is amenable to immunomodulatory therapy.

2021-02-22 | GSE161654 | GEO

Protein local synthesis at synapse is required for neuromuscular transmission

Project description:Protein local synthesis at synapse is required for neuromuscular transmission

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Local calcium accumulations promote phagocyte-mediated synapse removal in cortical neuroinflammation

Project description:Local calcium accumulations promote phagocyte-mediated synapse removal in cortical neuroinflammation

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Protein local synthesis at synapse is required for neuromuscular transmission

Project description:To profile the local translatome at the neuromuscular junction during various developmental stages We conducted RNA sequencing of synapse-enriched regions in the mouse diaphragms of both cre- and cre+ mice to investigate the local translatome at motor neuron terminals

2024-08-26 | GSE238144 | GEO

Chromatin remodeler Arid1a regulates subplate neuron identity and wiring of cortical connectivity

Project description:Loss-of-function mutations in chromatin remodeler gene ARID1A are a cause of Coffin-Siris syndrome, a developmental disorder characterized by dysgenesis of corpus callosum. Here, we characterize Arid1a function during cortical development and find unexpectedly selective roles for Arid1a in subplate neurons. Subplate neurons (SPNs), strategically positioned at the interface of cortical grey and white matter, orchestrate multiple developmental processes indispensable for neural circuit wiring. We find that pan-cortical deletion of Arid1a leads to extensive mistargeting of intracortical axons and agenesis of corpus callosum. Sparse Arid1a deletion, however, does not autonomously misroute callosal axons, implicating non-cell autonomous Arid1a functions in axon guidance. Supporting this possibility, the ascending axons of thalamocortical neurons, which are not autonomously affected by cortical Arid1a deletion, are also disrupted in their pathfinding into cortex and innervation of whisker barrels. Coincident with these miswiring phenotypes, which are reminiscent of subplate ablation, we unbiasedly find a selective loss of SPN gene expression following Arid1a deletion. In addition, multiple characteristics of SPNs crucial to their wiring functions, including subplate organization, subplate-thalamocortical axon co-fasciculation (“handshake”), and extracellular matrix, are severely disrupted. To empirically test Arid1a sufficiency in subplate, we generate a cortical plate deletion of Arid1a that spares SPNs. In this model, subplate Arid1a expression is sufficient for subplate-thalamocortical axon co-fasciculation and extracellular matrix assembly. Consistent with these wiring functions, subplate Arid1a sufficiently enables normal callosum formation, thalamocortical axon targeting, and whisker barrel development. Thus, Arid1a is a multifunctional regulator of subplate-dependent guidance mechanisms essential to cortical circuit wiring.

2021-05-06 | GSE163273 | GEO

Identification of genes involved in GABAergic Wiring

Project description:How neurons are wired to form precise circuits is crucial to understand the development of cortical functions. Glutamatergic pyramidal cell and GABAergic interneuron wire up the cortex through differentiated cellular events. However, little is known about the molecular mechanisms that underlie the unique features of interneuron wiring. We performed a high-throughput genomic screen for genes upregulated specifically during GABAergic wiring.

2018-07-31 | GSE115948 | GEO

Distinct molecular programs regulate synapse specificity in cortical inhibitory circuits

Project description:Distinct molecular programs regulate synapse specificity in cortical inhibitory circuits

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Transcriptomic Cell Type Specificity of Local Cortical Circuits

Project description:Transcriptomic Cell Type Specificity of Local Cortical Circuits

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Distinct molecular programs regulate synapse specificity in cortical inhibitory circuits

Project description:How neuronal connections are established and organized in functional networks determines brain function. In the mouse cerebral cortex, different classes of GABAergic interneurons exhibit specific connectivity patterns that underlie their ability to shape temporal dynamics and information processing. Much progress has been made parsing interneuron diversity, yet the molecular mechanisms by which interneuron subtype-specific connectivity motifs emerge remain unclear. Here we investigate transcriptional dynamics in different classes of interneurons during the formation of cortical inhibitory circuits. We found that whether the interneurons synapse with pyramidal neurons on their dendrites, soma, or axon initial segment is determined by synaptic molecules that are expressed in a subtype-specific manner. Thus cell-specific molecular programs that unfold during early postnatal development underlie the connectivity patterns of cortical interneurons.

2019-01-25 | GSE120161 | GEO

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