Neonatal exposure to an inflammatory cytokine, epidermal growth factor, results in the deficits of mismatch negativity in rats.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
16 05 2019
Historique:
received: 23 08 2018
accepted: 30 04 2019
entrez: 18 5 2019
pubmed: 18 5 2019
medline: 21 10 2020
Statut: epublish

Résumé

Perinatal exposure to epidermal growth factor (EGF) induces various cognitive and behavioral abnormalities after maturation in non-human animals, and is used for animal models of schizophrenia. Patients with schizophrenia often display a reduction of mismatch negativity (MMN), which is a stimulus-change specific event-related brain potential. Do the EGF model animals also exhibit the MMN reduction as schizophrenic patients do? This study addressed this question to verify the pathophysiological validity of this model. Neonatal rats received repeated administration of EGF or saline and were grown until adulthood. Employing the odd-ball paradigm of distinct tone pitches, tone-evoked electroencephalogram (EEG) components were recorded from electrodes on the auditory and frontal cortices of awake rats, referencing an electrode on the frontal sinus. The amplitude of the MMN-like potential was significantly reduced in EGF-treated rats compared with saline-injected control rats. The wavelet analysis of the EEG during a near period of tone stimulation revealed that synchronization of EEG activity, especially with beta and gamma bands, was reduced in EGF-treated rats. Results suggest that animals exposed to EGF during a perinatal period serve as a promising neurodevelopmental model of schizophrenia.

Identifiants

pubmed: 31097747
doi: 10.1038/s41598-019-43923-y
pii: 10.1038/s41598-019-43923-y
pmc: PMC6522493
doi:

Substances chimiques

Epidermal Growth Factor 62229-50-9

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

7503

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Auteurs

Eiichi Jodo (E)

Department of Systems Neuroscience, Fukushima Medical University School of Medicine, Fukushima, 960-1295, Japan. jodo1019@fmu.ac.jp.

Hiroyoshi Inaba (H)

Department of Molecular Neurobiology, Brain Research Institute, Niigata University, Niigata, 951-8585, Japan.

Itaru Narihara (I)

Department of Molecular Neurobiology, Brain Research Institute, Niigata University, Niigata, 951-8585, Japan.

Hidekazu Sotoyama (H)

Department of Molecular Neurobiology, Brain Research Institute, Niigata University, Niigata, 951-8585, Japan.

Eiko Kitayama (E)

Department of Molecular Neurobiology, Brain Research Institute, Niigata University, Niigata, 951-8585, Japan.

Hirooki Yabe (H)

Department of Neuropsychiatry, Fukushima Medical University School of Medicine, Fukushima, 960-1295, Japan.

Hisaaki Namba (H)

Department of Molecular Neurobiology, Brain Research Institute, Niigata University, Niigata, 951-8585, Japan.

Satoshi Eifuku (S)

Department of Systems Neuroscience, Fukushima Medical University School of Medicine, Fukushima, 960-1295, Japan.

Hiroyuki Nawa (H)

Department of Molecular Neurobiology, Brain Research Institute, Niigata University, Niigata, 951-8585, Japan.

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Classifications MeSH