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viernes, 11 de febrero de 2011

Función Mitocondrial y Neuroplasticidad

1. Nucleolus   2. Nucleus
   3. Ribosome
   4. Vesicle
   5. Rough endoplasmic reticulum
   6. Golgi apparatus (or "Golgi body")
   7. Cytoskeleton
   8. Smooth endoplasmic reticulum
   9. Mitochondrion
  10. Vacuole
  11. Cytosol
  12. Lysosome
  13. Centriole

Mitochondria and neuroplasticity Aiwu Cheng*1, Yan Hou* and Mark P Mattson*

*Laboratory of Neurosciences, National Institute of Aging Intramural Research Program, Baltimore, MD 21224, U.S.A.
{Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, U.S.A.
Cite this article as: Cheng A, Hou Y and Mattson MP (2010) Mitochondria and neuroplasticity. ASN NEURO 2(5):art:e00045.doi:10.1042/AN20100019

Figure 2 Molecular machinery that actively moves mitochondria to and fro within axons
A major mechanism by which mitochondria are transported in either anterograde or retrograde directions in axons involves their energy (ATP)-dependent movement along microtubules. ATP-dependent ‘motor’ proteins interact with the microtubules to generate the force that moves the mitochondria in anterograde (kinesin) or retrograde (dynein) directions respectively. Several APs (adaptor proteins) mediate the interaction of mitochondria with motor proteins, including APs that interact with kinesin (Milton, syntabulin and the Rho GTPase Miro) and APs that associate with dynein (dynactin). In addition, in synaptic terminals and growth cones, microtubules may be moved by myosin-mediated interactions with actin filaments. Myosin V can drive short-range movements along F-actin, as well as modulate long-range transport by pulling mitochondria away from microtubules by facilitating anchorage of mitochondria to F-actin by unknown actin–mitochondrion crosslinkers.

Figure 3 The landscape of mitochondrial involvement in the plasticity of neuronal structure and information processing Increasing evidence suggests that mitochondria play active roles in regulating the outgrowth of axons and dendrites, synaptogenesis and morphological and functional responses to synaptic activity. Mitochondria in presynaptic terminals (1) provide the energy for the maintenance and restoration of membrane potential, and may modulate neurotransmitter packaging and release. Mitochondria in postsynaptic spines (2) and dendritic shafts (3) may enable/regulate both structural and functional responses of these compartments to synaptic activity. Mitochondria in the cell body (4) provide the energy required for numerous biochemical processes, and may also serve as signalling platforms involved in information transfer within the neuron. Mitochondria in axons (5) provide the energy necessary for the transport of various proteins and organelles from the axon terminal to the cell body and vice versa.


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 Ca2+ 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

Key words: neural progenitor cell, mitochondria biogenesis, mitochondria fission and fusion.

Saludos cordiales/Gustavo