Figure 2.

N-acetylaspartate depletion occurs in the injured hemisphere of the rat brain 24 h and 2 weeks after TBI

MALDI-MS images for N-acetylaspartate (NAA, m/z (M-H) = 174.02) in (A) sham, (B) TBI at 24 h, and (C) TBI at 2 weeks.

(A) The green areas represent areas of elevated NAA in portions of the neocortex, thalamus, hypothalamus, and amygdala. The sham animal has a symmetric distribution between hemispheres.

(B) 24 h post injury, there is a reduction of NAA in the injured (left) and contralateral (right) neocortex. There is a dark region which represents the lesion site in the injured hemisphere and an area of little to no NAA. The thalamic and hypothalamic levels of NAA seem to be unaffected by TBI at the 24 h time point.

(C) 2 weeks post injury there is much more symmetry between the injured and contralateral hemisphere. However, there is still a small observed region in the neocortex and caudoputamen where NAA is reduced. (A–C) A representative scale bar of 5 mm is shown in white on the right hand-side mid-figure. Data are shown using a rainbow scale, normalized against total ion current.

(D and E) (D) The scanned image of the TBI brain and (E) overlaid with labels for general regions and the lesion site (LS) comprised of portions of the neocortex (CTX), caudoputamen (CP), corpus callosum (CC), and fimbria (Fi). (D and E) A representative scale bar of 5 mm is shown in white on the lower right-hand corner.