Aluminum-induced dendritic pathology revisited: cytochemical and electron microscopic studies of rabbit cortical pyramidal neurons.

Intracisternal administration of aluminum maltolate induces biochemical and histological changes in the rabbit brain. The primary histological response to this aluminum intoxication is the appearance within many neuronal somata and dendrites of intensely argyrophilic masses of fibrillar material. Ultrastructural examination of these bodies in both conventionally-prepared and silver-stained sections shows them to be composed of neurofilaments. For this reason, we have elected to call these argyrophilic masses "neurofilamentous arrays (NFAs)." At their zenith, NFAs in cortical pyramidal neurons comprise thousands of filaments interconnected by periodic crossbridges. NFAs begin to be formed within both somata and dendrites as isolated groups of neurofilaments, which apparently go on to assemble en masse within the cytoplasm. In symptomatic animals, many cortical neurons are rich in NFAs, yet lack classic cytological signs of degeneration, such as nuclear pyknosis. Though silver staining reveals extensive NFAs only in aluminum-exposed brains, there is a strong degree of immunostaining for phosphorylated neurofilamentous epitopes in both untreated and Al-injected animals. This suggests that protein subunits that are already present in the neurons under normal circumstances are recruited, in the presence of aluminum, to form NFAs through the directed assembly of masses of oriented filaments.