Synaptic activity becomes excitotoxic in neurons exposed to elevated levels of platelet-activating factor.

ABSTRACT: Neurologic impairment in HIV-1-associated dementia (HAD) and other neuroinflammatory diseases correlates with injury to dendrites and synapses, but how such injury occurs is not known. We hypothesized that neuroinflammation makes dendrites susceptible to excitotoxic injury following synaptic activity. We report that platelet-activating factor, an inflammatory phospholipid that mediates synaptic plasticity and neurotoxicity and is dramatically elevated in the brain during HAD, promotes dendrite injury following elevated synaptic activity and can replicate HIV-1-associated dendritic pathology. In hippocampal slices exposed to a stable platelet-activating factor analogue, tetanic stimulation that normally induces long-term synaptic potentiation instead promoted development of calcium- and cas

SUBMITTER: Bellizzi MJ 

PROVIDER: S-EPMC1265873 | biostudies-literature | 2005 Nov

REPOSITORIES: biostudies-literature