title: Synaptic plasticity in the pathophysiology and treatment of bipolar disorder.
abstract: Emerging evidence suggests that synaptic plasticity is intimately involved in the pathophysiology and treatment of bipolar disorder (BPD). Under certain conditions, over-strengthened and/or weakened synapses at different circuits in the brain could disturb brain functions in parallel, causing manic-like or depressive-like behaviors in animal models. In this chapter, we summarize the regulation of synaptic plasticity by medications, psychological conditions, hormones, and neurotrophic factors, and their correlation with mood-associated animal behaviors. We conclude that increased serotonin, norepinephrine, dopamine, brain-derived neurotrophic factor (BDNF), acute corticosterone, and antidepressant treatments lead to enhanced synaptic strength in the hippocampus and also correlate with antidepressant-like behaviors. In contrast, inhibiting monoaminergic signaling, long-term stress, and pathophysiological concentrations of cytokines weakens glutamatergic synaptic strength in the hippocampus and is associated with depressive-like symptoms.
authors.affiliation: Laboratory of Molecular Pathophysiology, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, 9000 Rockville Pike, Building 35, 1BC909, Bethesda, MD, 20892, USA, duj@mail.nih.gov.
authors.forename: Jing
authors.initials: J
authors.lastname: Du
authors.forename: Rodrigo
authors.initials: R
authors.lastname: Machado-Vieira
authors.forename: Rushaniya
authors.initials: R
authors.lastname: Khairova
mesh_terms: D000818:Animals; D000928:Antidepressive Agents / Q000627:therapeutic use; D001714:Bipolar Disorder / Q000473:pathology; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism; D004195:Disease Models, Animal; D006624:Hippocampus / Q000503:physiopathology; D006801:Humans; D009473:Neuronal Plasticity; D013569:Synapses
chemical_list: D000928:Antidepressive Agents; D019208:Brain-Derived Neurotrophic Factor