Abnormal development of zinc-containing cortical circuits in the absence of the transcription factor Tailless

Brain Res Dev Brain Res. 2005 Aug 8;158(1-2):97-101. doi: 10.1016/j.devbrainres.2005.04.006.


Absence of the transcription factor tailless (tlx) leads to premature laminar development and thinning of neocortex. We used zinc autometallography to determine if tailless deletion alters the organization of cortical circuits. In tlx-/- mice, layer 4 barrels, which normally lack synaptic zinc, are densely innervated by zinc-containing terminals. Furthermore, barrels with zinc inputs are constructed, in part, from zinc-sequestering neurons, a phenotype not normally found in layer 4.

Publication types

  • Comparative Study
  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Histocytochemistry / methods
  • Mice
  • Mice, Knockout
  • Nerve Net / abnormalities*
  • Nerve Net / metabolism*
  • Neurons / metabolism
  • Neurons / pathology
  • Receptors, Cytoplasmic and Nuclear / deficiency*
  • Somatosensory Cortex / abnormalities
  • Somatosensory Cortex / metabolism*
  • Somatosensory Cortex / pathology
  • Zinc / metabolism*


  • Nr2e1 protein, mouse
  • Receptors, Cytoplasmic and Nuclear
  • Zinc