Borna disease virus infection impairs synaptic plasticity.
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.
Volmer
Romain
R
INSERM U563, Centre de Physiopathologie de Toulouse Purpan, 31024 Toulouse Cedex 3, France.
Prat
Christine M A
CM
Le Masson
Gwendal
G
Garenne
André
A
Gonzalez-Dunia
Daniel
D
D000818:Animals; D001890:Borna Disease / Q000503:physiopathology*; D001891:Borna disease virus; D002540:Cerebral Cortex / Q000503:physiopathology* / Q000821:virology; D004594:Electrophysiology; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D009473:Neuronal Plasticity; D009474:Neurons / Q000821:virology; D010750:Phosphoproteins / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D013569:Synapses / Q000821:virology*; D009435:Synaptic Transmission; D015678:Viral Structural Proteins / Q000378:metabolism
C496537:P protein, Borna disease virus; D010750:Phosphoproteins; D015678:Viral Structural Proteins; D048049:Extracellular Signal-Regulated MAP Kinases