Deprivation and denervation differentially affect zinc-containing circuitries in the barrel cortex of mice.

In the neocortex, a population of glutamatergic synapses contains chelatable zinc that is released upon depolarization. The present study compares the effect of chronic tactile deprivation and vibrissectomy performed at different postnatal ages on the synaptic zinc distribution in the mouse barrel cortex. We found that a chronic unilateral tactile deprivation resulted in an increase of synaptic zinc in deprived barrels. Distribution and intensity of zinc staining in non-deprived barrels resembled the control situation. The increase of zinc staining was observed if chronic deprivation started in early postnatal life or in adolescent mice but not in 70-day-old animals. This suggests that a critical period exists for plasticity of zinc containing terminals in the barrel cortex. The alteration of zinc staining was localized to not only the thalamorecipient layers IV but also layer II/III, and upper layer V. Neonatal denervation of selected vibrissal rows resulted in rearrangement of synaptic zinc distribution following cytoarchitectonic alterations in the barrel field. However, no changes in the intensity of zinc staining were observed. Vibrissectomy performed after the critical period for barrel formation did not affect either the distribution or intensity of zinc staining. It appears that the integrity of vibrissa-barrel pathway is necessary to induce activity-dependent alterations in synaptic zinc.