• Monika Liguz-Lecznar, Dorota Nowicka, Artur Czupryn, and Jolanta Skangiel-Kramska.
• Laboratory of the Molecular Basis of Brain Plasticity, Department of Molecular and Cellular Neurobiology, Nencki Institute of Experimental Biology, 3 Pasteur St., 02-093 Warsaw, Poland.
• Brain Res. Bull. 2005 Jul 30; 66 (2): 106-13.

AbstractIn the neocortex, synaptic zinc level is regulated by sensory experience. Previously, we found that trimming of mystacial vibrissae resulted in an increase of synaptic zinc level in corresponding deprived barrels in the cortex of mice. The present study focused on the relationship between synaptic zinc and zinc transporter 3 (ZnT3) protein expression in the barrel cortex of mice during postnatal development and after sensory deprivation of selected vibrissae. Using immunocytochemistry and western blot analysis, we found that ZnT3 expression is delayed as compared with the onset of synaptic zinc and presynaptic markers, such as synapsin I and synaptophysin. Further, neither long-term deprivation in young mice nor short deprivation in adult mice, that resulted in an increase of synaptic zinc level, produced alterations in ZnT3, synapsin I or synaptophysin expression in deprived barrels. These results suggest that in the barrel cortex ZnT3, synapsin I or synaptophysin are not determinant for the activity-dependent regulation of the synaptic zinc level.

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