R
Robert Schwarcz
Researcher at University of Maryland, Baltimore
Publications - 368
Citations - 28632
Robert Schwarcz is an academic researcher from University of Maryland, Baltimore. The author has contributed to research in topics: Kynurenic acid & Quinolinic acid. The author has an hindex of 85, co-authored 362 publications receiving 26946 citations. Previous affiliations of Robert Schwarcz include Mitsubishi Tanabe Pharma & Karolinska Institutet.
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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.
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Lesion of striatal neurones with kainic acid provides a model for Huntington's chorea.
Joseph T. Coyle,Robert Schwarcz +1 more
TL;DR: It is reported that the injection of kainic acid into the rat striatum causes neuronal degeneration, neurochemical alterations and behavioural responses resembling Huntington's chorea, which could provide an animal model for the study of the disease.
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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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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.
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Blood–Brain Barrier Transport of Kynurenines: Implications for Brain Synthesis and Metabolism
TL;DR: The results demonstrate the saturable transfer of L‐KYN across the blood–brain barrier and suggest that circulating L‐ KYN, 3‐HKYN, and ANA may each contribute significantly to respective cerebral pools under normal conditions.