UNIGE document Scientific Article
previous document  unige:111467  next document
add to browser collection

Restoring wild-type-like CA1 network dynamics and behavior during adulthood in a mouse model of schizophrenia

Published in Nature neuroscience. 2018, vol. 21, no. 10, p. 1412-1420
Abstract Schizophrenia is a severely debilitating neurodevelopmental disorder. Establishing a causal link between circuit dysfunction and particular behavioral traits that are relevant to schizophrenia is crucial to shed new light on the mechanisms underlying the pathology. We studied an animal model of the human 22q11 deletion syndrome, the mutation that represents the highest genetic risk of developing schizophrenia. We observed a desynchronization of hippocampal neuronal assemblies that resulted from parvalbumin interneuron hypoexcitability. Rescuing parvalbumin interneuron excitability with pharmacological or chemogenetic approaches was sufficient to restore wild-type-like CA1 network dynamics and hippocampal-dependent behavior during adulthood. In conclusion, our data provide insights into the network dysfunction underlying schizophrenia and highlight the use of reverse engineering to restore physiological and behavioral phenotypes in an animal model of neurodevelopmental disorder.
Keywords Mental disorderSchizophreniaParvalbumin interneuronDesynchonization
Full text
Article (Published version) (11.4 MB) - document accessible for UNIGE members only Limited access to UNIGE
Other version: http://www.nature.com/articles/s41593-018-0225-y
Research groups Groupe Carleton Alan (neurosciences fondamentales) (876)
Groupe Rodriguez
(ISO format)
MARISSAL, Thomas et al. Restoring wild-type-like CA1 network dynamics and behavior during adulthood in a mouse model of schizophrenia. In: Nature Neuroscience, 2018, vol. 21, n° 10, p. 1412-1420. doi: 10.1038/s41593-018-0225-y https://archive-ouverte.unige.ch/unige:111467

464 hits



Deposited on : 2018-11-27

Export document
Format :
Citation style :