Abstract
Dynamic metabolic changes occurring in neurons are critically important in directing brain plasticity and cognitive function. In other tissue types, disruptions to metabolism and the resultant changes in cellular oxidative state, such as increased reactive oxygen species (ROS) or induction of hypoxia, are associated with cellular stress. In the brain however, where drastic metabolic shifts occur to support physiological processes, subsequent changes to cellular oxidative state and induction of transcriptional sensors of oxidative stress likely play a significant role in regulating physiological neuronal function. Understanding the role of metabolism and metabolically-regulated genes in neuronal function will be critical in elucidating how cognitive functions are disrupted in pathological conditions where neuronal metabolism is affected. Here, we discuss known mechanisms regulating neuronal metabolism as well as the role of hypoxia and oxidative stress during normal and disrupted neuronal function. We also summarize recent studies implicating a role for metabolism in regulating neuronal plasticity as an emerging neuroscience paradigm.
Highlights
Regulation of tissue metabolite supply and cellular energy metabolism is essential to maintain healthy cellular and systemic function
This synergistic function of astrocytes and neurons in Cerebral blood flow (CBF) regulation is mirrored in their inverse yet complimentary metabolic profiles with astrocytes predominantly metabolizing glucose via glycolysis while neurons rely on oxidative metabolism (Kasischke et al, 2004)
While neurovascular coupling mechanisms appear to maintain steady-state oxygen levels in the brain, it is becoming evident that neurovascular uncoupling may have a physiological role in regulating plasticity via oxygen depletion and induction of downstream hypoxia response pathways
Summary
Regulation of tissue metabolite supply and cellular energy metabolism is essential to maintain healthy cellular and systemic function. It is estimated that neurons consume 75%–80% of energy produced in the brain (Hyder et al, 2013) This energy is primarily utilized at the synapse with a large proportion spent in restoration of neuronal membrane potentials following depolarization (Harris et al, 2012). Other neuronal functions such as vesicle recycling, neurotransmitter synthesis and axoplasmic transport. While mechanisms have been identified to modify oxygen supply to brain regions in response to activity there appears to be a role for hypoxia in modulating neuronal function and behavior. In recent years a number of studies have identified links between metabolically regulated genes and behavior, which may provide insight into understanding the role of neuronal oxidative metabolism in both health and disease
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