Synaptic Signals from Glutamate-Treated Neurons Induce Aberrant Post-Synaptic Signals in Untreated Neuronal Networks

Glutamate neurotoxicity is associated with a wide range of disorders and can impair synaptic function. Failure to clear extracellular glutamate fosters additional cycles and spread of regional hyperexcitation.

Using cultured murine cortical neurons, herein it is demonstrated that synaptic signals generated by cultures undergoing glutamate-induced hyperactivity can invoke similar effects in other cultures not exposed to elevated glutamate.

Since sequential synaptic connectivity can encompass extensive cortical regions, this study presents a potential additional contributor to the spread of damage resulting from glutamate excitotoxicity and should be considered in attempts to mitigate neurodegeneration.