{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Xiong A"],"funding":["HHS | NIH | National Institute of Neurological Disorders and Stroke (NINDS)","NIAAA NIH HHS","NINDS NIH HHS","HHS | NIH | National Institute on Alcohol Abuse and Alcoholism (NIAAA)","NIH HHS"],"pagination":["e2404969121"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11363341"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["121(35)"],"pubmed_abstract":["The abundance of CaV2 voltage-gated calcium channels is linked to presynaptic homeostatic plasticity (PHP), a process that recalibrates synaptic strength to maintain the stability of neural circuits. However, the molecular and cellular mechanisms governing PHP and CaV2 channels are not completely understood. Here, we uncover a previously not described form of PHP in <i>Caenorhabditis elegans</i>, revealing an inverse regulatory relationship between the efficiency of neurotransmitter release and the abundance of UNC-2/CaV2 channels. Gain-of-function <i>unc-2SL(S240L)</i> mutants, which carry a mutation analogous to the one causing familial hemiplegic migraine type 1 in humans, showed markedly reduced channel abundance despite increased channel functionality. Reducing synaptic release in the"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Presynaptic neurons self-tune by inversely coupling neurotransmitter release with the abundance of CaV2 voltage-gated Ca&lt;sup&gt;2+&lt;/sup&gt; channels."],"pmcid":["PMC11363341"],"funding_grant_id":["R21 AA029811","R21AA029811","R21 NS139113","R21NS139113","P40 OD010440"],"pubmed_authors":["Kim H","Xiong A","Richmond JE"],"additional_accession":[]},"is_claimable":false,"name":"Presynaptic neurons self-tune by inversely coupling neurotransmitter release with the abundance of CaV2 voltage-gated Ca&lt;sup&gt;2+&lt;/sup&gt; channels.","description":"The abundance of CaV2 voltage-gated calcium channels is linked to presynaptic homeostatic plasticity (PHP), a process that recalibrates synaptic strength to maintain the stability of neural circuits. However, the molecular and cellular mechanisms governing PHP and CaV2 channels are not completely understood. Here, we uncover a previously not described form of PHP in <i>Caenorhabditis elegans</i>, revealing an inverse regulatory relationship between the efficiency of neurotransmitter release and the abundance of UNC-2/CaV2 channels. Gain-of-function <i>unc-2SL(S240L)</i> mutants, which carry a mutation analogous to the one causing familial hemiplegic migraine type 1 in humans, showed markedly reduced channel abundance despite increased channel functionality. Reducing synaptic release in the","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Aug","modification":"2025-04-03T23:17:00.539Z","creation":"2025-04-03T23:17:00.539Z"},"accession":"S-EPMC11363341","cross_references":{"pubmed":["39172783"],"doi":["10.1073/pnas.2404969121"]}}