Journal ArticleDOI
Increased cortical kynurenate content in schizophrenia.
Robert Schwarcz,Arash Rassoulpour,Hui Qiu Wu,Deborah R. Medoff,Carol A. Tamminga,Rosalinda C. Roberts +5 more
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TLDR
In rats, chronic treatment with haloperidol did not cause an increase in kynurenate levels in the frontal cortex, indicating that the elevation observed in schizophrenia is not due to antipsychotic medication.About:
This article is published in Biological Psychiatry.The article was published on 2001-10-01. It has received 538 citations till now. The article focuses on the topics: Kynurenate & Kynurenine aminotransferase II.read more
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Mammalian nicotinic acetylcholine receptors: from structure to function.
TL;DR: This review provides a comprehensive overview of the advancement of functional and genetic studies in the late 1980s and the more recent revelations of the impact that the rich diversity in function and expression of this receptor family has on neuronal and nonneuronal cells throughout the body.
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Kynurenines in the mammalian brain: when physiology meets pathology
TL;DR: With recently developed pharmacological agents, it is now possible to restore metabolic equilibrium and envisage novel therapeutic interventions on the basis of the kynurenine pathway.
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Glutamate and Schizophrenia: Beyond the Dopamine Hypothesis
TL;DR: Hypofunction of the NMDA receptor, possibly on critical GABAergic inter-neurons, may contribute to the pathophysiology of schizophrenia.
Journal ArticleDOI
The Brain Metabolite Kynurenic Acid Inhibits α7 Nicotinic Receptor Activity and Increases Non-α7 Nicotinic Receptor Expression: Physiopathological Implications
Corey Hilmas,Edna F. R. Pereira,Manickavasagom Alkondon,Arash Rassoulpour,Robert Schwarcz,Edson X. Albuquerque +5 more
TL;DR: It is demonstrated that nAChRs are targets for KYNA and suggest a functionally significant cross talk between the nicotinic cholinergic system and the kynurenine pathway in the brain.
Journal ArticleDOI
Autism-like behavioral phenotypes in BTBR T+tf/J mice
Hewlet G. McFarlane,G. K. Kusek,Mu Yang,J. L. Phoenix,V. J. Bolivar,V. J. Bolivar,Jacqueline N. Crawley +6 more
TL;DR: Robust and selective social deficits, repetitive self‐grooming, genetic stability and commercial availability of the BTBR inbred strain encourage its use as a research tool to search for background genes relevant to the etiology of autism, and to explore therapeutics to treat the core symptoms.
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Journal Article
Protein Measurement with the Folin Phenol Reagent
TL;DR: Procedures are described for measuring protein in solution or after precipitation with acids or other agents, and for the determination of as little as 0.2 gamma of protein.
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Subanesthetic effects of the noncompetitive NMDA antagonist, ketamine, in humans: Psychotomimetic, perceptual, cognitive, and neuroendocrine responses.
John H. Krystal,Laurence P. Karper,John Seibyl,Glenna K. Freeman,Richard C. Delaney,J. Douglas Bremner,George R. Heninger,Malcolm B. Bowers,Dennis S. Charney +8 more
TL;DR: These data indicate that N-methyl-D-aspartate antagonists produce a broad range of symptoms, behaviors, and cognitive deficits that resemble aspects of endogenous psychoses, particularly schizophrenia and dissociative states.
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Glutamate receptor dysfunction and schizophrenia.
John W. Olney,Nuri B. Farber +1 more
TL;DR: It is proposed that since N-methyl-D-aspartate receptor hypofunction can cause psychosis in humans and corticolimbic neurodegenerative changes in the rat brain, and since these changes are prevented by certain antipsychotic drugs, including atypical neuroleptic agents, a better understanding of this mechanism may lead to improved pharmacotherapy in schizophrenia.
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The dissociative anaesthetics, ketamine and phencyclidine, selectively reduce excitation of central mammalian neurones by N-methyl-aspartate
TL;DR: The results suggest that reduction of synaptic excitation mediated via NMA receptors contributes to the anaesthetic/analgesic properties of these two dissociative anaesthetics.
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Quinolinic acid: an endogenous metabolite that produces axon-sparing lesions in rat brain
TL;DR: Intracerebral injection of the neuroexcitatory tryptophan metabolite, quinolinic acid, has behavioral, neurochemical and neuropathological consequences reminiscent of those of exogenous excitotoxins, such as kainic and ibotenic acids.