T opical application of potassium chloride solutions (above 0·25 M) as well as some other agents onto the surface of the brain cortex provokes typical changes in the basic performance of the brain. Serious impairment of learning as well as depression of spontaneous activity, depolarization of the cortical cells, disappearance of the evoked responses, changes in unit activity and alteration of energy metabolism are among the detectable features of this phenomenon called cortical spreading depression (CSD) by its discoverer LEÃ (1944). For reviews on CSD see M arshall (1959); B urést (1962); O chs (1962). The inhibitory effect of CSD on the incorporation of the labelled amino acids into the proteins of the rat cerebral cortex has been reported (R uščák 1964; B ennett and E delman , 1969; K řivánek , 1969, 1970) and the distribution of the effect among the crude subcellular fractions was studied by K řivánek (1970). Possible involvement of macromolecules, particularly proteins in memory formation and storage has been claimed. It was tempting to see whether the proteins of some mitochondrial subfractions namely nerve endings particles and pure mitochondria, could reveal a differential susceptibility to the potassium action which, in vivo , induces such profound changes in the brain cortex function.
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Avaria et al. (1973) studied this question.
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