Redox dysregulation, neuroinflammation, and NMDA receptor hypofunction: A “central hub” in schizophrenia pathophysiology?-Reference-Cited by-同舟云学术

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Redox dysregulation, neuroinflammation, and NMDA receptor hypofunction: A “central hub” in schizophrenia pathophysiology?

Published:2016-09 Issue:1 Volume:176 Page:41-51
ISSN:0920-9964
Container-title:Schizophrenia Research
language:en
Short-container-title:Schizophrenia Research

Author:

Steullet P.,Cabungcal J.H.,Monin A.,Dwir D.,O'Donnell P.,Cuenod M.,Do K.Q.

Funder

Swiss National Science Foundation

National Center of Competence in Research (NCCR)

Avina Foundation

Damm-Etienne Foundation

Loterie Romande

Alamaya Foundation

University of Maryland School of Medicine

National Institute of Mental Health

NARSAD

Publisher

Elsevier BV

Subject

Biological Psychiatry,Psychiatry and Mental health

Reference231 articles.

1. Prenatal exposure to an NMDA receptor antagonist, MK-801 reduces density of parvalbumin-immunoreactive GABAergic neurons in the medial prefrontal cortex and enhances phencyclidine-induced hyperlocomotion but not behavioral sensitization to methamphetamine in postpubertal rats

2. Parvalbumin-expressing interneurons linearly transform cortical responses to visual stimuli;Atallah;Neuron,2012

3. N-acetylcysteine—a safe antidote for cysteine/glutathione deficiency;Atkuri;Curr. Opin. Pharmacol.,2007

4. H2O2 signaling in the nigrostriatal dopamine pathway via ATP-sensitive potassium channels: issues and answers;Avshalumov;Antioxid. Redox Signal.,2007

5. Maturation-dependent vulnerability of oligodendrocytes to oxidative stress-induced death caused by glutathione depletion;Back;J. Neurosci.,1998

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