Recovery versus death of "dark" (compacted) neurons in non-impaired parenchymal environment: light and electron...

The formation of massively shrunken, hyperbasophilic, hyperargyrophilic and hyper-electron-dense but not apoptotic ("dark") neurons was initiated in rat brains by means of an electric-shock and two mechanical-injury paradigms that do not cause considerable parenchymal damage in the areas investigated. The rats were killed by perfusion fixation either immediately after these instantaneous initiating insults or after a survival period ranging from 40 min to 6 days. The formation of "dark" neurons was complete in less than a few minutes. In the somatodendritic domain of each "dark" neuron, all ultrastructural elements were remarkably preserved during the acute stage, apart from a dramatic reduction of the distances between them. This ultrastructural compaction was accompanied by a marked shift of cell fluid through seemingly intact plasma membrane, mainly into surrounding astrocytic elements. The majority of the "dark" neurons regained their normal morphology and staining properties (recovery) in 4 h. Thereafter, only solitary mitochondrion-derived membranous whorls in the cytoplasm reminded of a previous morphological disturbance. The dead "dark" neurons fell apart into membrane-bound fragments that retained their sharp outlines and compacted interior even after being engulfed by astrocytes or microglial cells. The latter sequence of morphological changes can not be harmonized with the prevailing assumption, according to which "dark" neurons die through the necrotic pathway. The fate of the "dark" neurons appeared to depend on the presence or absence of serious post-insult pathophysiological circumstances in their surroundings.