{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chang YC"],"funding":["HHS | National Institutes of Health","NINDS NIH HHS"],"pagination":["e2315958121"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11032469"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["121(16)"],"pubmed_abstract":["The ability of neurons to rapidly remodel their synaptic structure and strength in response to neuronal activity is highly conserved across species and crucial for complex brain functions. However, mechanisms required to elicit and coordinate the acute, activity-dependent structural changes across synapses are not well understood, as neurodevelopment and structural plasticity are tightly linked. Here, using an RNAi screen in <i>Drosophila</i> against genes affecting nervous system functions in humans, we uncouple cellular processes important for synaptic plasticity and synapse development. We find mutations associated with neurodegenerative and mental health disorders are 2-times more likely to affect activity-induced synaptic remodeling than synapse development. We report that while both "],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Identification of secretory autophagy as a mechanism modulating activity-induced synaptic remodeling."],"pmcid":["PMC11032469"],"funding_grant_id":["R01 NS102260","R01NS102260","R01NS080946","R01 NS080946"],"pubmed_authors":["Langen J","Gao Y","Peng YJ","Lee JY","Chang KT","Chang YC"],"additional_accession":[]},"is_claimable":false,"name":"Identification of secretory autophagy as a mechanism modulating activity-induced synaptic remodeling.","description":"The ability of neurons to rapidly remodel their synaptic structure and strength in response to neuronal activity is highly conserved across species and crucial for complex brain functions. However, mechanisms required to elicit and coordinate the acute, activity-dependent structural changes across synapses are not well understood, as neurodevelopment and structural plasticity are tightly linked. Here, using an RNAi screen in <i>Drosophila</i> against genes affecting nervous system functions in humans, we uncouple cellular processes important for synaptic plasticity and synapse development. We find mutations associated with neurodegenerative and mental health disorders are 2-times more likely to affect activity-induced synaptic remodeling than synapse development. We report that while both ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Apr","modification":"2026-06-07T07:40:26.589Z","creation":"2025-04-05T18:42:38.815Z"},"accession":"S-EPMC11032469","cross_references":{"pubmed":["38588427"],"doi":["10.1073/pnas.2315958121"]}}