Neuronal correlates of an encephalopathy associated with aluminum neurofibrillary degeneration.
A previous study reported that the intracranial injection of a soluble aluminum salt induced an encephalopathy which may serve as a useful animal model of dementia. An early sign of the encephalopathy in cats was a progressive decrement in both the performance of a short-term visual retention task and acquisition of a conditioned avoidance response in the presence of normal visual discrimination. This study reports that 10 days following the application of aluminum (AlCl3) there was an absence in cat visual cortex of neurons with spontaneous frequencies between 7 and 12 spikes/sec. The loss was associated with neurofibrillary degeneration and aluminum concentrations in lateral gyrus between 4 and 6 mug/g dry weight. The remaining neurons decreased their variability of response to identical visual stimuli and increased their probability of response and frequency of discharge.
D000535:Aluminum / Q000032:analysis / Q000506:poisoning*; D000818:Animals; D001921:Brain / Q000648:ultrastructure; D001923:Brain Chemistry; D001927:Brain Diseases / Q000139:chemically induced* / Q000473:pathology; D002415:Cats; D005071:Evoked Potentials; D006801:Humans; D008569:Memory Disorders / Q000139:chemically induced* / Q000473:pathology; D009454:Neurofibrils / Q000648:ultrastructure*; D011930:Reaction Time; D014793:Visual Cortex / Q000503:physiopathology*; D014796:Visual Perception
D000535:Aluminum