• Post-mortem experiments;
  • “Dark” neurons;
  • Ultrastructural compaction;
  • Non-enzymatic mechanism;
  • Stored non-covalent free energy


At the end of transcardial perfusions with ice-cold physiological saline for 30 min or with isoosmotic potassium chloride for 5 min, but immediately before perfusion fixation, condenser-discharge electric shocks were administered to rats through surface electrodes pressed onto the temporal muscles of the scalped skull. As a result, striking ultrastructural compaction came about in numerous neurons thinly scattered in certain brain areas. Its features displayed a high degree of similarity to those previously observed following the in vivo administration of the same kind of electric shocks. This surprising independence from the actual state of metabolism questions whether the ultrastructural compaction, induced either in vivo or post mortem, is the result of any cascade of enzyme-mediated processes. On the other hand, a physical mechanism, phase transition propagated by non-covalent free energy stored in a cytoplasmic gel structure, which was proposed recently to explain a mechanically induced similar ultrastructural compaction, appears to apply also to the present case.