Journal ArticleDOI
Quinolinic acid: an endogenous metabolite that produces axon-sparing lesions in rat brain
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TLDR
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.Abstract:
A current hypothesis links the neuroexcitatory properties of certain acidic amino acids to their ability to cause selective neuronal lesions. 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. Its qualities as a neurotoxic agent suggest that quinolinic acid should be considered as a possible pathogenic factor in neurodegenerative disorders.read more
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A Meta-Analysis of Cytokines in Major Depression
Yekta Dowlati,Nathan Herrmann,Nathan Herrmann,Walter Swardfager,Walter Swardfager,Helena Liu,Lauren Sham,Elyse K. Reim,Krista L. Lanctôt,Krista L. Lanctôt +9 more
TL;DR: A meta-analysis of studies measuring cytokine concentration in patients with major depression reports significantly higher concentrations of the proinflammatory cytokines TNF-alpha and IL-6 in depressed subjects compared with control subjects, strengthening evidence that depression is accompanied by activation of the IRS.
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Blockade of N-methyl-D-aspartate receptors may protect against ischemic damage in the brain.
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Limbic seizure and brain damage produced by kainic acid: Mechanisms and relevance to human temporal lobe epilepsy
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Glutamate as a Neurotransmitter in the Brain: Review of Physiology and Pathology
TL;DR: Endogenous glutamate, by activating NMDA, AMPA or mGluR1 receptors, may contribute to the brain damage occurring acutely after status epilepticus, cerebral ischemia or traumatic brain injury, and may also contribute to chronic neurodegeneration in such disorders as amyotrophic lateral sclerosis and Huntington's chorea.
References
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Journal ArticleDOI
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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Duplication of biochemical changes of Huntington's chorea by intrastriatal injections of glutamic and kainic acids
TL;DR: This work has injected 1 µl of either kainic acid or L-glutamic acid dissolved in isotonic saline directly into the extrapyramidal nuclei of rats, and found that injection into the striatum produced local enzymatic changes duplicating those reported in Huntington's chorea.
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Cytotoxic effects of acidic and sulphur containing amino acids on the infant mouse central nervous system
TL;DR: The close correspondence in molecular specificities associated with neurotoxic and neuroexcitatory properties of simple amino acids suggests the two phenomena may be governed by similar mechanisms of action.
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Quinolinic acid: a potent endogenous excitant at amino acid receptors in CNS.
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Intraventricular kainic acid preferentially destroys hippocampal pyramidal cells.
TL;DR: The results suggest that kainic acid lesions can provide a model of hippocampal damage in man and the unusual sensitivity of CA3–CA4, and to a lesser extent CA1, pyramidal cells to this agent is reported.