Mitochondria and neuroplasticity

ASN Neuro. 2010 Oct 4;2(5):e00045. doi: 10.1042/AN20100019.

Abstract

The production of neurons from neural progenitor cells, the growth of axons and dendrites and the formation and reorganization of synapses are examples of neuroplasticity. These processes are regulated by cell-autonomous and intercellular (paracrine and endocrine) programs that mediate responses of neural cells to environmental input. Mitochondria are highly mobile and move within and between subcellular compartments involved in neuroplasticity (synaptic terminals, dendrites, cell body and the axon). By generating energy (ATP and NAD(+)), and regulating subcellular Ca(2+) and redox homoeostasis, mitochondria may play important roles in controlling fundamental processes in neuroplasticity, including neural differentiation, neurite outgrowth, neurotransmitter release and dendritic remodelling. Particularly intriguing is emerging data suggesting that mitochondria emit molecular signals (e.g. reactive oxygen species, proteins and lipid mediators) that can act locally or travel to distant targets including the nucleus. Disturbances in mitochondrial functions and signalling may play roles in impaired neuroplasticity and neuronal degeneration in Alzheimer's disease, Parkinson's disease, psychiatric disorders and stroke.

Keywords: AD, Alzheimer's disease; AP, adaptor protein; APP, amyloid precursor protein; Aβ, amyloid β-peptide; BDNF, brain-derived neurotrophic factor; CR, caloric restriction; CREB, cAMP-response-element-binding protein; CaMK, Ca2+/calmodulin-dependent protein kinase; ES, embryonic stem; ETC, electron transport chain; HD, Huntington's disease; LRRK2, leucine-rich repeat kinase 2; LTP, long-term potentiation; MAPK, mitogen-activated protein kinase; Mn-SOD, manganese superoxide dismutase; NGF, nerve growth factor; NMDA, N-methyl-d-aspartate; Nrf1, nuclear respiratory factor 1; OPA1, Optic Atrophy-1; PD, Parkinson's disease; PGC1α, peroxisome-proliferator-activated receptor γ co-activator 1α; PINK1, PTEN (phosphatase and tensin homologue deleted on chromosome 10)-induced kinase 1; PPAR, peroxisome-proliferator-activated receptor; UCP, uncoupling protein; mitochondria biogenesis; mitochondria fission and fusion; neural progenitor cell.

Publication types

  • Review

MeSH terms

  • Alzheimer Disease / metabolism
  • Alzheimer Disease / pathology
  • Animals
  • Humans
  • Mitochondria / metabolism*
  • Mitochondria / pathology
  • Mitochondria / physiology
  • Neurogenesis / physiology
  • Neuronal Plasticity / physiology*
  • Neurons / cytology
  • Neurons / metabolism*
  • Neurons / pathology
  • Parkinson Disease / metabolism
  • Parkinson Disease / pathology
  • Synaptic Transmission / physiology