{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Moujaes F"],"funding":["Usona Institute","NCATS NIH HHS","National Institute on Alcohol Abuse and Alcoholism","NIMH NIH HHS","Brain and Behavior Research Foundation","NIAAA NIH HHS","National Institutes of Health","Heffter Research Institute","Simons Foundation Autism Research Initiative","Swiss Neuromatrix Foundation","Swiss National Science Foundation under the framework of Neuron Cofund","NIH HHS","National Science Foundation"],"pagination":["e84173"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11023699"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13"],"pubmed_abstract":["<h4>Background</h4>Ketamine has emerged as one of the most promising therapies for treatment-resistant depression. However, inter-individual variability in response to ketamine is still not well understood and it is unclear how ketamine's molecular mechanisms connect to its neural and behavioral effects.<h4>Methods</h4>We conducted a single-blind placebo-controlled study, with participants blinded to their treatment condition. 40 healthy participants received acute ketamine (initial bolus 0.23 mg/kg, continuous infusion 0.58 mg/kg/hr). We quantified resting-state functional connectivity via data-driven global brain connectivity and related it to individual ketamine-induced symptom variation and cortical gene expression targets.<h4>Results</h4>We found that: (i) both the neural and behavior"],"journal":["eLife"],"pubmed_title":["Ketamine induces multiple individually distinct whole-brain functional connectivity signatures."],"pmcid":["PMC11023699"],"funding_grant_id":["2015 - 2056","2015276","U01 MH121766","Pilot Award","R01 MH108590","R01 MH112746","01EW1908","UL1 TR001863","R01 MH112189","1-190420","5R01MH112189","5R01MH108590","DP5 OD012109","Young Investigator Award","2016-0111","P50 AA012870","R01MH112746","2P50AA012870-11","1U01MH121766","DP5OD012109-01"],"pubmed_authors":["Vollenweider FX","Murray JD","Morgan PT","Rieser N","Adkinson BD","Diehl C","Krystal JH","Camarro T","Savic A","Flynn M","Seifritz E","Kolobaric A","Anticevic A","Repovs G","Tamayo Z","Ji JL","Cho Y","Moujaes F","Santamauro N","Xu J","Schleifer C","Rahmati M","Fonteneau C","Burt JB","Fineberg SK","Preller KH"],"additional_accession":[]},"is_claimable":false,"name":"Ketamine induces multiple individually distinct whole-brain functional connectivity signatures.","description":"<h4>Background</h4>Ketamine has emerged as one of the most promising therapies for treatment-resistant depression. However, inter-individual variability in response to ketamine is still not well understood and it is unclear how ketamine's molecular mechanisms connect to its neural and behavioral effects.<h4>Methods</h4>We conducted a single-blind placebo-controlled study, with participants blinded to their treatment condition. 40 healthy participants received acute ketamine (initial bolus 0.23 mg/kg, continuous infusion 0.58 mg/kg/hr). We quantified resting-state functional connectivity via data-driven global brain connectivity and related it to individual ketamine-induced symptom variation and cortical gene expression targets.<h4>Results</h4>We found that: (i) both the neural and behavior","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Apr","modification":"2026-06-02T10:26:23.966Z","creation":"2025-04-06T00:48:44.866Z"},"accession":"S-EPMC11023699","cross_references":{"pubmed":["38629811"],"doi":["10.7554/eLife.84173"]}}