{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Parekh PK"],"funding":["NIMH NIH HHS","NINDS NIH HHS"],"pagination":["581-601"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11577286"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["45"],"pubmed_abstract":["Depression is an episodic form of mental illness characterized by mood state transitions with poorly understood neurobiological mechanisms. Antidepressants reverse the effects of stress and depression on synapse function, enhancing neurotransmission, increasing plasticity, and generating new synapses in stress-sensitive brain regions. These properties are shared to varying degrees by all known antidepressants, suggesting that synaptic remodeling could play a key role in depression pathophysiology and antidepressant function. Still, it is unclear whether and precisely how synaptogenesis contributes to mood state transitions. Here, we review evidence supporting an emerging model in which depression is defined by a distinct brain state distributed across multiple stress-sensitive circuits, with neurons assuming altered functional properties, synapse configurations, and, importantly, a reduced capacity for plasticity and adaptation. Antidepressants act initially by facilitating plasticity and enabling a functional reconfiguration of this brain state. Subsequently, synaptogenesis plays a specific role in sustaining these changes over time."],"journal":["Annual review of neuroscience"],"pubmed_title":["Synaptic Mechanisms Regulating Mood State Transitions in Depression."],"pmcid":["PMC11577286"],"funding_grant_id":["R01 MH123154","R01 MH118451","RF1 NS126073","R01 MH109685"],"pubmed_authors":["Parekh PK","Johnson SB","Liston C"],"additional_accession":[]},"is_claimable":false,"name":"Synaptic Mechanisms Regulating Mood State Transitions in Depression.","description":"Depression is an episodic form of mental illness characterized by mood state transitions with poorly understood neurobiological mechanisms. Antidepressants reverse the effects of stress and depression on synapse function, enhancing neurotransmission, increasing plasticity, and generating new synapses in stress-sensitive brain regions. These properties are shared to varying degrees by all known antidepressants, suggesting that synaptic remodeling could play a key role in depression pathophysiology and antidepressant function. Still, it is unclear whether and precisely how synaptogenesis contributes to mood state transitions. Here, we review evidence supporting an emerging model in which depression is defined by a distinct brain state distributed across multiple stress-sensitive circuits, with neurons assuming altered functional properties, synapse configurations, and, importantly, a reduced capacity for plasticity and adaptation. Antidepressants act initially by facilitating plasticity and enabling a functional reconfiguration of this brain state. Subsequently, synaptogenesis plays a specific role in sustaining these changes over time.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jul","modification":"2025-04-26T01:52:49.328Z","creation":"2025-04-06T10:17:19.301Z"},"accession":"S-EPMC11577286","cross_references":{"pubmed":["35508195"],"doi":["10.1146/annurev-neuro-110920-040422"]}}