Aluminum induced neurofibrillary degeneration, brain electrical activity and alterations in acquisition and retention

The disorganization of the dendritic microtubular system is postulated to alter dendroplasmic flow and supports the hypothesis that the translocation of synaptically active agents by the cytoplasmic streaming mechanism may subserve a component of the associative learning mechanism.

Abstract

In the early stages of an aluminum induced dementia model a positive correlation exists between the occurrence of neurofibrillary degeneration (NFD) in hippocampus, entorhinal and neocortex and the rate of conditioned avoidance response acquisition. Quantitative measurements from appropriate electronmicrographs indicate that the density of microtubules in a region of NFD is profoundly reduced. At the stage in the encephalopathy in which short-term retention and acquisition are impaired the EEG and averaged visual evoked potentials were normal. The observations suggest that a nonelectrical activity of neurons, important to the learning-memory mechanism, may be altered by the effects of aluminum chloride. The disorganization of the dendritic microtubular system is postulated to alter dendroplasmic flow and supports the hypothesis that the translocation of synaptically active agents by the cytoplasmic streaming mechanism may subserve a component of the associative learning mechanism.