Borna disease virus infection impairs synaptic plasticity
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Updated: Jul 14, 2026

Intracerebroventricular Viral Injection of the Neonatal Mouse Brain for Persistent and Widespread Neuronal Transduction
Published on: September 15, 2014
Romain Volmer1, Christine M A Prat, Gwendal Le Masson
1INSERM U563, Centre de Physiopathologie de Toulouse Purpan, 31024 Toulouse Cedex 3, France.
Abstract:
The mechanisms whereby Borna disease virus (BDV) can impair neuronal function and lead to neurobehavioral disease are not well understood. To analyze the electrophysiological properties of neurons infected with BDV, we used cultures of neurons grown on multielectrode arrays, allowing a real-time monitoring of the electrical activity across the network shaped by synaptic transmission. Although infection did not affect spontaneous neuronal activity, it selectively blocked activity-dependent enhancement of neuronal network activity, one form of synaptic plasticity thought to be important for learning and memory. These findings highlight the original mechanism of the neuronal dysfunction caused by noncytolytic infection with BDV.
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