Abstract
Neuronal dysfunction in experimental aluminum encephalopathy has been attributed to aluminum-induced neurofibrillary degeneration and the resultant neuronal loss. We observed a marked decline in neuronal function in the in vitro hippocampal slice taken from animals at various stages of the experimental encephalopathy. Extracellular evoked-potential analysis of the CA1 subfield revealed marked uncoupling of orthodromic spike generation and a decreased ability to demonstrate long-term potentiation. These effects were progressive and occurred in the absence of neurofibrillary degeneration.
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