PubMed · 10375897
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S Izumo. 1999-05-10. [AIDS encephalopathy].. https://pubmed.ncbi.nlm.nih.gov/10375897/
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Inflammation and associated excitotoxicity may play important roles in various neurodegenerative diseases including AIDS dementia. Here we show that exposure of rat parietal cortical slices to the HIV glycoproteins gp120 and gp41 triggered very rapid releases of the neurotransmitters glutamate and [(3)H]noradrenaline (NA), and of the neuromodulator adenosine. Gp41 was more effective than gp120 at releasing glutamate and [(3)H]NA, while both glycoproteins were equi-effective at releasing adenosine. The responses to gp120 and gp41 declined rapidly to basal levels following their removal. It seems possible that rapid, inappropriate excitation may occur in the immediate vicinity of HIV infections in the brain, possibly producing some of the transient neurological and psychiatric symptoms associated with AIDS dementia.
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HIV infection at late stages is associated with neurological complications including impaired motor and cognitive functions. We used simian immunodeficiency (SIV)-infected rhesus monkeys, an animal model of HIV infection, to investigate changes in choline acetyltransferase (ChAT) activity, a biochemical marker of cognitive function, in post-mortem brains during early, asymptomatic SIV infection and AIDS. ChAT activity was dramatically reduced in putamen and hippocampus already during asymptomatic infection. In animals with AIDS, ChAT activity was further decreased. The reduction of ChAT was not related to brain viral load or CNS pathological lesions. Our results demonstrate deficits in ChAT activity already during the first months of SIV infection and imply that cognitive dysfunction may occur early in immunodeficiency viral infections.