The fate of "dark" neurons produced by transient focal cerebral ischemia in a non-necrotic and non-excitotoxic environment: neurobiological aspects.
BACKGROUND
We recently proposed novel neurobiological ideas for discussion regarding the common nature (malfunction of a physicochemical phenomenon genetically programmed for the morphological execution of ontogenetic apoptosis), mechanism of formation (phase transition in an intraneuronal gel structure) and mode of death (neither necrosis nor apoptosis) of "dark" neurons. These ideas were deduced from morphological changes in neurons found in a visually undamaged environment after in vivo or postmortem mechanical or electric injuries and after hypoglycemia.


OBJECTIVE
In search of further support, this paper revisits these ideas in the case of transient focal cerebral ischemia by investigating the light- and electron-microscopic changes produced in neurons by a 1-h occlusion of the rat middle cerebral artery in non-necrotic and non-excitotoxic tissue areas, where extraneuronal pathological processes may not influence the intraneuronal events.


RESULTS
In the first hour after restoration of circulation, the soma-dendrite domains of "dark" neurons displayed hyperbasophilia, hyperargyrophilia, hyper-electron density and a dramatic compaction of ultrastructural elements. Between 1 h and 1 day of the restored circulation, the degree of ultrastructural compaction decreased and mitochondrion-derived membranous whorls appeared in several "dark" neurons indicating recovery. Further, the cytoplasm of scattered neurons manifesting the apoptotic condensation pattern of the nuclear chromatin displayed the same morphological features as those of the freshly produced "dark" neurons. After 1 day of restored circulation, both the non-recovering "dark" neurons and the apoptotic neurons fell into membrane-bound, compact and electron-dense fragments, which were subsequently engulfed by phagocytotic cells.


CONCLUSIONS
These observations support each of the ideas mentioned above.
Kövesdi
Erzsébet
E
Department of Neurosurgery, Pécs University, H-7624 Pécs, Rét utca 2, Hungary.
Pál
József
J
Gallyas
Ferenc
F
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001921:Brain / Q000473:pathology / Q000648:ultrastructure*; D016923:Cell Death / Q000502:physiology*; D004195:Disease Models, Animal; D002546:Ischemic Attack, Transient / Q000473:pathology*; D008297:Male; D009474:Neurons / Q000145:classification / Q000473:pathology / Q000648:ultrastructure*; D051381:Rats; D017208:Rats, Wistar