THE ENDOGENEOUS AGONIST QUINOLINIC ACID AND THE NON ENDOGENOUS HOMOQUINOLINIC ACID DISCRIMINATE BETWEEN NMDAR2 RECEPTOR SUBUNITS

@article{Carvalho1996THEEA,
  title={THE ENDOGENEOUS AGONIST QUINOLINIC ACID AND THE NON ENDOGENOUS HOMOQUINOLINIC ACID DISCRIMINATE BETWEEN NMDAR2 RECEPTOR SUBUNITS},
  author={Lia Prado de Carvalho and Pascal Bochet and Jean Rossier},
  journal={Neurochemistry International},
  year={1996},
  volume={28},
  pages={445-452}
}
Ethanol Differentially Inhibits Homoquinolinic Acid- and NMDA-Induced Neurotoxicity in Primary Cultures of Cerebellar Granule Cells
TLDR
The results suggest that HQ reveals either a novel site or a not previously observed mechanism of interaction between ethanol and NMDA receptors in rat cerebellar granule cell cultures.
Quinolinic Acid: An Endogenous Neurotoxin with Multiple Targets
TLDR
Some of the most relevant targets of QUIN neurotoxicity which involves presynaptic receptors, energetic dysfunction, oxidative stress, transcription factors, cytoskeletal disruption, behavior alterations, and cell death are described.
N‐Methyl‐d‐aspartate receptor subtype‐selectivity of homoquinolinate: an electrophysiological and radioligand binding study using both native and recombinant receptors
TLDR
It is shown that NMDA‐specific [3H]homoquinolinate binding to rat brain membranes comprised 44% of total binding with a Bmax value of 5.73 pmol/mg protein, which was inhibited by NMDA with Ki=0.867 µm, and electrophysiological experiments suggest that homoquinolinated is not highly selective for NR2B‐containing receptors.
Quinolinate and related excitotoxins: mechanisms of neurotoxicity and disease relevance
TLDR
The data accumulated to date make a strong case for this hitherto obscure pathway being a major factor in determining cell damage, death, or recovery in health and disease.
Cinnabarinic acid and xanthurenic acid : two unorthodox kynurenine metabolites that interact with metabotropic glutamate receptors
TLDR
The growing interest on these two “unorthodox” metabolites of the kynurenine pathway may unravel new aspects in the complex interaction between tryptophan metabolism and brain function, and lead to the discovery of new potential targets for the treatment of neurological and psychiatric disorders.
3‐Hydroxykynurenine potentiates quinolinate but not NMDA toxicity in the rat striatum
TLDR
Data indicate that an elevation of L‐3‐HK levels constitutes a significant hazard in situations of excitotoxic injury, and pharmacological interventions aimed at decreasing L‐ 3‐HK formation may therefore be particularly useful for the treatment of neurological diseases which are associated with an abnormally enhanced flux through the kynurenine pathway.
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