Abnormal development of zinc-containing cortical circuits in the absence of the transcription factor Tailless.
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.
Land
Peter W
PW
Department of Neurobiology, W1458 Biomedical Science Tower, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA. pland@pitt.edu
Monaghan
A Paula
AP
D000818:Animals; D006651:Histocytochemistry / Q000379:methods; D051379:Mice; D018345:Mice, Knockout; D009415:Nerve Net / Q000002:abnormalities* / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D018160:Receptors, Cytoplasmic and Nuclear / Q000172:deficiency*; D013003:Somatosensory Cortex / Q000002:abnormalities / Q000378:metabolism* / Q000473:pathology; D015032:Zinc / Q000378:metabolism*
C490258:Nr2e1 protein, mouse; D018160:Receptors, Cytoplasmic and Nuclear; D015032:Zinc