作者: Ferenc Gallyas , Attila Csord�s , Attila Schwarcz , M�ria M�zl�
DOI: 10.1007/S00221-004-2037-4
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摘要: “Dark” neurons were produced in the cortex of rat brain by hypoglycemic convulsions. In somatodendritic domain each affected neuron, ultrastructural elements, except for disturbed mitochondria, remarkably preserved during acute stage, but distances between them reduced dramatically (ultrastructural compaction). Following a 1-min convulsion period, only few involved and their environment appeared undamaged. contrast, 1-h convulsions many caused swelling astrocytic processes neuronal dendrites (excitotoxic neuropil). A proportion “dark” recovered normal structure 2 days. The non-recovering removed from through two entirely different pathways. case convulsions, organelles swelled, then disintegrated finally dispersed into neuropil large gaps plasma membrane (necrotic-like removal). fell apart membrane-bound fragments that retained compacted interior even after being engulfed astrocytes or microglial cells (apoptotic-like Consequently, contrast to what is generally accepted, do not die as consequence necrosis. As regards it assumed necrotic-like removal process imposed, an excitotoxic environment, on previously died non-necrotic pathway. Apoptotic hippocampal dentate gyrus intraventricularly administered colchicine. After biochemical had been completed chromatin condensation nucleus reached advanced phase, elements cytoplasm became compacted. If present apparently undamaged such apoptotic sequence morphological changes, whereas those impaired changes. This suggests pathway may depend death pathway, also