BCL-xL regulates synaptic plasticity

Mol Interv. 2006 Aug;6(4):208-22. doi: 10.1124/mi.6.4.7.

Abstract

Mitochondria are the predominant organelle within many presynaptic terminals. During times of high synaptic activity, they affect intracellular calcium homeostasis and provide the energy needed for synaptic vesicle recycling and for the continued operation of membrane ion pumps. Recent discoveries have altered our ideas about the role of mitochondria in the synapse. Mitochondrial localization, morphology, and docking at synaptic sites may indeed alter the kinetics of transmitter release and calcium homeostasis in the presynaptic terminal. In addition, the mitochondrial ion channel BCL-xL, known as a protector against programmed cell death, regulates mitochondrial membrane conductance and bioenergetics in the synapse and can thereby alter synaptic transmitter release and the recycling of pools of synaptic vesicles. BCL-xL, therefore, not only affects the life and death of the cell soma, but its actions in the synapse may underlie the regulation of basic synaptic processes that subtend learning, memory and synaptic development.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis / physiology
  • Axons / physiology
  • Calcium / physiology
  • Cytoskeletal Proteins / genetics
  • Cytoskeletal Proteins / physiology
  • Drosophila / physiology
  • GTP-Binding Proteins / genetics
  • GTP-Binding Proteins / physiology
  • Mitochondria / physiology
  • Mutation
  • Neuronal Plasticity*
  • Neurons / physiology*
  • Synapses / physiology*
  • Synaptic Transmission
  • Synaptic Vesicles / physiology
  • Voltage-Dependent Anion Channels / physiology
  • bcl-X Protein / biosynthesis
  • bcl-X Protein / physiology*

Substances

  • Cytoskeletal Proteins
  • Voltage-Dependent Anion Channels
  • bcl-X Protein
  • DRP1 protein, Drosophila
  • GTP-Binding Proteins
  • Calcium