Interneuron hypomyelination is associated with cognitive inflexibility in a rat model of schizophrenia

Dorien A. Maas (), Vivian D. Eijsink, Marcia Spoelder, Josephus A. Hulten, Peter Weerd, Judith R. Homberg, Astrid Vallès, Brahim Nait-Oumesmar () and Gerard J. M. Martens ()
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Dorien A. Maas: Radboud University
Vivian D. Eijsink: Radboud University
Marcia Spoelder: Radboud University Medical Center
Josephus A. Hulten: Radboud University
Peter Weerd: Maastricht University
Judith R. Homberg: Radboud University Medical Center
Astrid Vallès: Radboud University
Brahim Nait-Oumesmar: Sorbonne Université, CNRS UMR 7225, Hôpital Pitié-Salpêtrière
Gerard J. M. Martens: Radboud University

Nature Communications, 2020, vol. 11, issue 1, 1-16

Abstract: Abstract Impaired cognitive functioning is a core feature of schizophrenia, and is hypothesized to be due to myelination as well as interneuron defects during adolescent prefrontal cortex (PFC) development. Here we report that in the apomorphine-susceptible (APO-SUS) rat model, which has schizophrenia-like features, a myelination defect occurred specifically in parvalbumin interneurons. The adult rats displayed medial PFC (mPFC)-dependent cognitive inflexibility, and a reduced number of mature oligodendrocytes and myelinated parvalbumin inhibitory axons in the mPFC. In the developing mPFC, we observed decreased myelin-related gene expression that persisted into adulthood. Environmental enrichment applied during adolescence restored parvalbumin interneuron hypomyelination as well as cognitive inflexibility. Collectively, these findings highlight that impairment of parvalbumin interneuron myelination is related to schizophrenia-relevant cognitive deficits.

Date: 2020
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DOI: 10.1038/s41467-020-16218-4

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