{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zubov T"],"funding":["NINDS NIH HHS","NIH HHS"],"pagination":["11610"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9270477"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(1)"],"pubmed_abstract":["Neural networks tune synaptic and cellular properties to produce stable activity. One form of homeostatic regulation involves scaling the strength of synapses up or down in a global and multiplicative manner to oppose activity disturbances. In American bullfrogs, excitatory synapses scale up to regulate breathing motor function after inactivity in hibernation, connecting homeostatic compensation to motor behavior. In traditional models of homeostatic synaptic plasticity, inactivity is thought to increase synaptic strength via mechanisms that involve reduced Ca<sup>2+</sup> influx through voltage-gated channels. Therefore, we tested whether pharmacological inactivity and inhibition of voltage-gated Ca<sup>2+</sup> channels are sufficient to drive synaptic compensation in this system. For th"],"journal":["Scientific reports"],"pubmed_title":["Inactivity and Ca<sup>2+</sup> signaling regulate synaptic compensation in motoneurons following hibernation in American bullfrogs."],"pmcid":["PMC9270477"],"funding_grant_id":["1R01NS114514","R15 NS112920"],"pubmed_authors":["Santin JM","Zubov T","do Amaral-Silva L"],"additional_accession":[]},"is_claimable":false,"name":"Inactivity and Ca<sup>2+</sup> signaling regulate synaptic compensation in motoneurons following hibernation in American bullfrogs.","description":"Neural networks tune synaptic and cellular properties to produce stable activity. One form of homeostatic regulation involves scaling the strength of synapses up or down in a global and multiplicative manner to oppose activity disturbances. In American bullfrogs, excitatory synapses scale up to regulate breathing motor function after inactivity in hibernation, connecting homeostatic compensation to motor behavior. In traditional models of homeostatic synaptic plasticity, inactivity is thought to increase synaptic strength via mechanisms that involve reduced Ca<sup>2+</sup> influx through voltage-gated channels. Therefore, we tested whether pharmacological inactivity and inhibition of voltage-gated Ca<sup>2+</sup> channels are sufficient to drive synaptic compensation in this system. For th","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jul","modification":"2025-05-18T11:54:05.296Z","creation":"2022-07-20T05:02:35.199Z"},"accession":"S-EPMC9270477","cross_references":{"pubmed":["35803955"],"doi":["10.1038/s41598-022-15525-8"]}}