Scientific article

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

Published inNature Neuroscience, vol. 21, no. 10, p. 1412-1420
Publication date2018

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.

  • Mental disorder
  • Schizophrenia
  • Parvalbumin interneuron
  • Desynchonization
Citation (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
Main files (1)
Article (Published version)
ISSN of the journal1097-6256

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