, Volume 116, Issue 4, pp 463-464

Aldehyde fixation is not necessary for the formation of “dark” neurons

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Kherani and Auer [6] recently reported a study in Acta Neuropathologica relating to the mechanism of the formation of “dark” neurons. Their observations led them to suggest that (1) both in vivo and during the early postmortem period, glutamate release and transmembrane ion fluxes cause some perturbation in a proportion of neurons, which become shrunken, hyperchromatic under the light microscope, and condensed, hyperelectron-dense at the ultrastructural level, but only while aldehyde fixation is underway, (2) the shrinkage/condensation is executed by transmembrane ion fluxes or by actin filaments, and (3) everything considered, the formation of “dark” neurons is a biotic process. This idea was logically deduced in part from the results of an experiment dealing with the formation of the artefactual “dark” neurons of Cammermeyer (i.e., neurons formed even in normal brain tissue when removed from the skull without previous transcardial aldehyde fixation followed by a 24-h delay [1]), and