Changes in the vesicular zinc pattern following traumatic brain injury

• DOI: 10.1016/j.neuroscience.2007.09.066
• Publication Date: 2007-10-11T12:54:46Z
• Authors: P. Doering; G. Danscher; A. Larsen; M. Bruhn; C. Søndergaard; M. Stoltenberg
• Keywords: Mice, Knockout; Neurons; Mice, Inbred BALB C; Time Factors; Membrane Proteins; Membrane Transport Proteins; Neocortex; Immunohistochemistry; Disease Models, Animal; Mice; Zinc; 03 medical and health sciences; 0302 clinical medicine; Brain Injuries; Animals; Synaptic Vesicles; Carrier Proteins; Microscopy, Immunoelectron; Cation Transport Proteins

The present study aims at evaluating the significance of zinc ions on the development of brain damage in a model of traumatic brain injury (TBI). The zinc ion specific autometallographic technique, the ZnSe(AMG) method, using silver enhancement of in vivo-captured zinc ions bound in zinc-selenium nanocrystals was applied to follow changes in the vesicular zinc pattern. Balb/c mice, ZnT3 knockout (ZnT3-Ko) mice, a mouse genetically knocked out for the protein ZnT3 responsible for sequestering zinc into synaptic vesicles, and littermates from the genetically un-manipulated mother type mice, wild type (Wt), were used. The Wt and the Balb/c mice exhibited instantaneously a boost in the zinc staining adjacent to the lesion involving all six neocortical layers. Ultra-structural analyses revealed that the in vivo created ZnSe nanocrystals were still confined to the vesicles of the zinc-enriched (ZEN) neurons in the neuropil. No differences between the Balb/c and Wt mice were seen at any time points. In the ZnT3-Ko mice the ZEN terminals stayed void of AMG grains, but a number of neuronal somata around the lesion became loaded with ZnSe nanocrystals. These silver-enhanced ZnSe nanocrystals were confined to the cytoplasm of the somata and their proximal dendrites. No such soma staining was seen in the Wt or Balb/c mice. We speculate that vesicular zinc may not contribute to neuronal damage following TBI.