Glutathione deficit during development induces anomalies in the rat anterior cingulate GABAergic neurons: Relevance to schizophrenia

Glutathione deficit during development induces anomalies in the rat anterior cingulate GABAergic neurons: Relevance to schizophrenia

A series of studies in schizophrenic patients report a decrease of glutathione (GSH) in prefrontal cortex (PFC) and cerebrospinal fluid, a decrease in mRNA levels for two GSH synthesizing enzymes and a deficit in parvalbumin (PV) expression in a subclass of GABA neurons in PFC. GSH is an important r...

Full description

Bibliographic Details
Main Authors: Jan-Harry Cabungcal, Dominique Nicolas, Rudolf Kraftsik, Michel Cuénod, Kim Q. Do, Jean-Pierre Hornung
Format: Article
Language:English
Published: Elsevier 2006-06-01
Series:Neurobiology of Disease
Subjects:
Animal model
Anterior cingulate cortex
γ-amino butyric acid
Glutathione
GBR 12909
Inhibitory interneurons
Online Access:http://www.sciencedirect.com/science/article/pii/S0969996106000052
id doaj-999449aba8544b3e8c6c6a43684c0078
record_format Article
spelling doaj-999449aba8544b3e8c6c6a43684c00782021-03-20T04:52:29ZengElsevierNeurobiology of Disease1095-953X2006-06-01223624637Glutathione deficit during development induces anomalies in the rat anterior cingulate GABAergic neurons: Relevance to schizophreniaJan-Harry Cabungcal0Dominique Nicolas1Rudolf Kraftsik2Michel Cuénod3Kim Q. Do4Jean-Pierre Hornung5Center for Research in Psychiatric Neuroscience, Department of Adult Psychiatry-CHUV, University of Lausanne, 1008-Prilly, Switzerland; Département de Biologie Cellulaire et de Morphologie, Faculty of Biology and Medicine, University of Lausanne, Switzerland; Corresponding author. Center for Research in Psychiatric Neuroscience, Department of Adult Psychiatry, University of Lausanne, 1008-Prilly, Switzerland. Fax: +41 21 643 6562.Département de Biologie Cellulaire et de Morphologie, Faculty of Biology and Medicine, University of Lausanne, SwitzerlandDépartement de Biologie Cellulaire et de Morphologie, Faculty of Biology and Medicine, University of Lausanne, SwitzerlandCenter for Research in Psychiatric Neuroscience, Department of Adult Psychiatry-CHUV, University of Lausanne, 1008-Prilly, SwitzerlandCenter for Research in Psychiatric Neuroscience, Department of Adult Psychiatry-CHUV, University of Lausanne, 1008-Prilly, SwitzerlandDépartement de Biologie Cellulaire et de Morphologie, Faculty of Biology and Medicine, University of Lausanne, SwitzerlandA series of studies in schizophrenic patients report a decrease of glutathione (GSH) in prefrontal cortex (PFC) and cerebrospinal fluid, a decrease in mRNA levels for two GSH synthesizing enzymes and a deficit in parvalbumin (PV) expression in a subclass of GABA neurons in PFC. GSH is an important redox regulator, and its deficit could be responsible for cortical anomalies, particularly in regions rich in dopamine innervation. We tested in an animal model if redox imbalance (GSH deficit and excess extracellular dopamine) during postnatal development would affect PV-expressing neurons. Three populations of interneurons immunolabeled for calcium-binding proteins were analyzed quantitatively in 16-day-old rat brain sections. Treated rats showed specific reduction in parvalbumin immunoreactivity in the anterior cingulate cortex, but not for calbindin and calretinin. These results provide experimental evidence for the critical role of redox regulation in cortical development and validate this animal model used in schizophrenia research.http://www.sciencedirect.com/science/article/pii/S0969996106000052Animal modelAnterior cingulate cortexγ-amino butyric acidGlutathioneGBR 12909Inhibitory interneurons
collection DOAJ
language English
format Article
sources DOAJ
author Jan-Harry Cabungcal
Dominique Nicolas
Rudolf Kraftsik
Michel Cuénod
Kim Q. Do
Jean-Pierre Hornung
spellingShingle Jan-Harry Cabungcal
Dominique Nicolas
Rudolf Kraftsik
Michel Cuénod
Kim Q. Do
Jean-Pierre Hornung
Glutathione deficit during development induces anomalies in the rat anterior cingulate GABAergic neurons: Relevance to schizophrenia
Neurobiology of Disease
Animal model
Anterior cingulate cortex
γ-amino butyric acid
Glutathione
GBR 12909
Inhibitory interneurons
author_facet Jan-Harry Cabungcal
Dominique Nicolas
Rudolf Kraftsik
Michel Cuénod
Kim Q. Do
Jean-Pierre Hornung
author_sort Jan-Harry Cabungcal
title Glutathione deficit during development induces anomalies in the rat anterior cingulate GABAergic neurons: Relevance to schizophrenia
title_short Glutathione deficit during development induces anomalies in the rat anterior cingulate GABAergic neurons: Relevance to schizophrenia
title_full Glutathione deficit during development induces anomalies in the rat anterior cingulate GABAergic neurons: Relevance to schizophrenia
title_fullStr Glutathione deficit during development induces anomalies in the rat anterior cingulate GABAergic neurons: Relevance to schizophrenia
title_full_unstemmed Glutathione deficit during development induces anomalies in the rat anterior cingulate GABAergic neurons: Relevance to schizophrenia
title_sort glutathione deficit during development induces anomalies in the rat anterior cingulate gabaergic neurons: relevance to schizophrenia
publisher Elsevier
series Neurobiology of Disease
issn 1095-953X
publishDate 2006-06-01
description A series of studies in schizophrenic patients report a decrease of glutathione (GSH) in prefrontal cortex (PFC) and cerebrospinal fluid, a decrease in mRNA levels for two GSH synthesizing enzymes and a deficit in parvalbumin (PV) expression in a subclass of GABA neurons in PFC. GSH is an important redox regulator, and its deficit could be responsible for cortical anomalies, particularly in regions rich in dopamine innervation. We tested in an animal model if redox imbalance (GSH deficit and excess extracellular dopamine) during postnatal development would affect PV-expressing neurons. Three populations of interneurons immunolabeled for calcium-binding proteins were analyzed quantitatively in 16-day-old rat brain sections. Treated rats showed specific reduction in parvalbumin immunoreactivity in the anterior cingulate cortex, but not for calbindin and calretinin. These results provide experimental evidence for the critical role of redox regulation in cortical development and validate this animal model used in schizophrenia research.
topic Animal model
Anterior cingulate cortex
γ-amino butyric acid
Glutathione
GBR 12909
Inhibitory interneurons
url http://www.sciencedirect.com/science/article/pii/S0969996106000052
work_keys_str_mv AT janharrycabungcal glutathionedeficitduringdevelopmentinducesanomaliesintheratanteriorcingulategabaergicneuronsrelevancetoschizophrenia
AT dominiquenicolas glutathionedeficitduringdevelopmentinducesanomaliesintheratanteriorcingulategabaergicneuronsrelevancetoschizophrenia
AT rudolfkraftsik glutathionedeficitduringdevelopmentinducesanomaliesintheratanteriorcingulategabaergicneuronsrelevancetoschizophrenia
AT michelcuenod glutathionedeficitduringdevelopmentinducesanomaliesintheratanteriorcingulategabaergicneuronsrelevancetoschizophrenia
AT kimqdo glutathionedeficitduringdevelopmentinducesanomaliesintheratanteriorcingulategabaergicneuronsrelevancetoschizophrenia
AT jeanpierrehornung glutathionedeficitduringdevelopmentinducesanomaliesintheratanteriorcingulategabaergicneuronsrelevancetoschizophrenia
_version_ 1724211935736496128

Similar Items