Serotonin, a phylogenetically ancient molecule that predates the evolution of the nervous system, was likely co-opted to function as a neurotransmitter. Serotonin retains “pre-nervous” trophic-factor actions influencing development and growth, while exerting pleiotropic neurotransmitter effects on diverse brain functions and behavior [1]. Serotonin is speculated to exert antioxidant-like actions [1]; however, its influence on the energy producing organelle, mitochondria, and on a neuron’s stress buffering capacity remains poorly understood.

Mitochondrial function is essential to fulfill substantial neuronal metabolic demands, maintain excitability, and facilitate synaptic transmission. Mitochondria serve as key signaling platforms, coupling metabolic status to mitochondrial dynamics, biogenesis and function, and influence neuronal metabolism, intracellular signaling, and synaptic plasticity [2]. Mitochondrial biogenesis is an adaptive mechanism that responds to cellular energetic demands and oxidative insults, and can promote neuronal viability. We hypothesized that serotonin in keeping with its putative trophic and antioxidant-like actions, may serve as an upstream modulator of mitochondria in neurons and thus influence stress buffering.

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