Brainstem Neurons Survive the Identical Ischemic Stress That Kills Higher Neurons: Insight to the Persistent Vegetative State
Figure 1
Light transmittance (LT) imaging reveals damage following AD in higher, but not lower, brain regions.
A) The front of LT change representing AD onset arises and propagates as distinct waves coursing through hippocampal and neocortical gray matter (arrows) leaving damage (light scatter, purple) in its wake. B) Palytoxin introduced at zero minutes induces OGD-like AD at extremely low concentrations by converting the Na+/K+ pump to cationic channel. The resulting LT front initiates in neocortex and then hippocampus. Note spreading swelling in the CA1 cell body layer (red). These cortical regions are subsequently damaged (purple). These findings were replicated in 30 of 30 slices using 10 or 1 nM palytoxin. With 0.1 nM palytoxin, AD was observed in 12 of 16 slices but rarely in subcortical regions [71]. C) In midbrain-pons, AD propagates as ‘mini-fronts’ through superior colliculus and PAG, causing swelling but no damage. Superficial superior colliculus is an exception (see Discussion). D) More caudally, AD swells and damages cerebellar gray, but only temporarily swells tegmental nuclei (TN) in the pons.