Experimental Brain Research

, Volume 160, Issue 4, pp 473–486

“Dark” (compacted) neurons may not die through the necrotic pathway


    • Department of Neurosurgery, Faculty of MedicinePécs University
  • Attila Csordás
    • Department of Neurosurgery, Faculty of MedicinePécs University
  • Attila Schwarcz
    • Department of Neurosurgery, Faculty of MedicinePécs University
  • Mária Mázló
    • Central Electron Microscopic Laboratory, Faculty of MedicinePécs University
Research Article

DOI: 10.1007/s00221-004-2037-4

Cite this article as:
Gallyas, F., Csordás, A., Schwarcz, A. et al. Exp Brain Res (2005) 160: 473. doi:10.1007/s00221-004-2037-4


“Dark” neurons were produced in the cortex of the rat brain by hypoglycemic convulsions. In the somatodendritic domain of each affected neuron, the ultrastructural elements, except for disturbed mitochondria, were remarkably preserved during the acute stage, but the distances between them were reduced dramatically (ultrastructural compaction). Following a 1-min convulsion period, only a few neurons were involved and their environment appeared undamaged. In contrast, 1-h convulsions affected many neurons and caused swelling of astrocytic processes and neuronal dendrites (excitotoxic neuropil). A proportion of “dark” neurons recovered the normal structure in 2 days. The non-recovering “dark” neurons were removed from the brain cortex through two entirely different pathways. In the case of 1-h convulsions, their organelles swelled, then disintegrated and finally dispersed into the neuropil through large gaps in the plasma membrane (necrotic-like removal). Following a 1-min convulsion period, the non-recovering “dark” neurons fell apart into membrane-bound fragments that retained the compacted interior even after being engulfed by astrocytes or microglial cells (apoptotic-like removal). Consequently, in contrast to what is generally accepted, the “dark” neurons produced by 1-min hypoglycemic convulsions do not die as a consequence of necrosis. As regards the case of 1-h convulsions, it is assumed that a necrotic-like removal process is imposed, by an excitotoxic environment, on “dark” neurons that previously died through a non-necrotic pathway. Apoptotic neurons were produced in the hippocampal dentate gyrus by intraventricularly administered colchicine. After the biochemical processes had been completed and the chromatin condensation in the nucleus had reached an advanced phase, the ultrastructural elements in the somatodendritic cytoplasm of the affected cells became compacted. If present in an apparently undamaged environment such apoptotic neurons were removed from the dentate gyrus through the apoptotic sequence of morphological changes, whereas those present in an impaired environment were removed through a necrotic-like sequence of morphological changes. This suggests that the removal pathway may depend on the environment and not on the death pathway, as also assumed in the case of the “dark” neurons produced by hypoglycemic convulsions.


Hypoglycemic convulsions“Dark” neuronsCell deathSilver stainingElectron microscopy

Copyright information

© Springer-Verlag 2004