Death receptor 6 regulates adult experience-dependent cortical plasticity

J Neurosci. 2013 Sep 18;33(38):14998-5003. doi: 10.1523/JNEUROSCI.2398-13.2013.

Abstract

Sensory experience alters cortical circuitry by parallel processes of axon outgrowth and pruning, but the mechanisms that control these rearrangements are poorly understood. Using in vivo 2-photon longitudinal imaging, we found a marked reduction in axonal pruning in somatosensory cortex of mice with a knock-out of the DR6 gene, which codes for Death Receptor 6. This effect was seen for both long-range horizontal excitatory connections and for the axons of inhibitory neurons. These results identify a new pathway governing axonal plasticity associated with experience-dependent changes in cortical maps.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Axons / physiology
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2 / genetics
  • Dependovirus
  • Glutamate Decarboxylase / genetics
  • Glutamate Decarboxylase / metabolism
  • Luminescent Proteins / genetics
  • Luminescent Proteins / metabolism
  • Mice
  • Mice, Knockout
  • Neural Inhibition / genetics
  • Neuronal Plasticity / genetics
  • Neuronal Plasticity / physiology*
  • Neurons / physiology*
  • Physical Stimulation
  • Presynaptic Terminals / physiology
  • Receptors, Tumor Necrosis Factor / deficiency
  • Receptors, Tumor Necrosis Factor / metabolism*
  • Somatosensory Cortex* / cytology
  • Somatosensory Cortex* / metabolism
  • Somatosensory Cortex* / physiology
  • Transduction, Genetic
  • Vibrissae / innervation*

Substances

  • Luminescent Proteins
  • Receptors, Tumor Necrosis Factor
  • Tnfrsf21 protein, mouse
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2
  • Camk2a protein, mouse
  • Glutamate Decarboxylase
  • glutamate decarboxylase 2