Abstract
New theories about the pathophysiology of depression and mechanisms of action of antidepressants proposes that regulation of intracellular signalling pathways manifested by disturbed neuroplasticity plays a critical role in higher-order brain functions. Mitochondria may be primary regulators of these processes.
It is supposed that mitochondrial dysfunctions are included in pathophysiology of mood disorders. Mitochondrial hypothesis of bipolar affective disorder corresponds to neurotrophic and neuroplasticity hypotheses because of an important role of mitochondria in cell energetic, regulation of calcium signalling pathway, production of reactive oxygen species and apoptosis, i.e. in processes determining synaptic plasticity, damage, repairing, survival or death of neurons.