Synaptic plasticity in the pathophysiology and treatment of bipolar disorder

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.