Acetylcholine content and distribution in rat cortical synaptosomes after in vivo exposure to quinolinic acid

1990 ◽  
Vol 108 (1-2) ◽  
pp. 219-224 ◽  
Author(s):  
Robert H. Metcalf ◽  
David L. Riddell ◽  
Roland J. Boegman
Keyword(s):  
Quinolinic Acid ◽  
Acetylcholine Content

scholarly journals Cerebral dopamine neurotrophic factor (CDNF) protects against quinolinic acid-induced toxicity in in vitro and in vivo models of Huntington’s disease

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
P. Stepanova ◽  
V. Srinivasan ◽  
D. Lindholm ◽  
M. H. Voutilainen
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Quinolinic Acid ◽  
Neurotrophic Factor ◽  
Striatal Neurons ◽  
In Vivo Models ◽  
Cerebral Dopamine Neurotrophic Factor ◽  
Cerebral Dopamine

Abstract Huntington’s disease (HD) is a neurodegenerative disorder with a progressive loss of medium spiny neurons in the striatum and aggregation of mutant huntingtin in the striatal and cortical neurons. Currently, there are no rational therapies for the treatment of the disease. Cerebral dopamine neurotrophic factor (CDNF) is an endoplasmic reticulum (ER) located protein with neurotrophic factor (NTF) properties, protecting and restoring the function of dopaminergic neurons in animal models of PD more effectively than other NTFs. CDNF is currently in phase I–II clinical trials on PD patients. Here we have studied whether CDNF has beneficial effects on striatal neurons in in vitro and in vivo models of HD. CDNF was able to protect striatal neurons from quinolinic acid (QA)-induced cell death in vitro via increasing the IRE1α/XBP1 signalling pathway in the ER. A single intrastriatal CDNF injection protected against the deleterious effects of QA in a rat model of HD. CDNF improved motor coordination and decreased ataxia in QA-toxin treated rats, and stimulated the neurogenesis by increasing doublecortin (DCX)-positive and NeuN-positive cells in the striatum. These results show that CDNF positively affects striatal neuron viability reduced by QA and signifies CDNF as a promising drug candidate for the treatment of HD.

N-Acetylaspartylglutamate (NAAG) protects against rat striatal quinolinic acid lesions in vivo

1997 ◽  
Vol 236 (2) ◽  
pp. 91-94 ◽  
Author(s):  
Lianna R. Orlando ◽  
Ruth Luthi-Carter ◽  
David G. Standaert ◽  
Joseph T. Coyle ◽  
John B. Penney ◽  
...  
Keyword(s):  
Quinolinic Acid

Quinolinic acid neurotoxicity: In vivo increased copper and manganese content in rat corpus striatum after quinolinate intrastriatal injection

1996 ◽  
Vol 87 (2-3) ◽  
pp. 113-119 ◽  
Author(s):  
Abel Santamaria ◽  
Camilo Rios ◽  
Patricia Pérez ◽  
Abigail Flores ◽  
Sonia Galván-Arzate ◽  
...  
Keyword(s):  
Quinolinic Acid ◽  
Corpus Striatum ◽  
Manganese Content ◽  
Intrastriatal Injection

scholarly journals Quinolinic Acid: An Endogenous Neurotoxin with Multiple Targets

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Rafael Lugo-Huitrón ◽  
Perla Ugalde Muñiz ◽  
Benjamin Pineda ◽  
José Pedraza-Chaverrí ◽  
Camilo Ríos ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nmda Receptor ◽  
Quinolinic Acid ◽  
Neurological Diseases ◽  
Presynaptic Receptors ◽  
Kynurenine Pathway ◽  
Uptake System ◽  
Neuronal Degradation ◽  
Cytoskeletal Disruption

Quinolinic acid (QUIN), a neuroactive metabolite of the kynurenine pathway, is normally presented in nanomolar concentrations in human brain and cerebrospinal fluid (CSF) and is often implicated in the pathogenesis of a variety of human neurological diseases. QUIN is an agonist of N-methyl-D-aspartate (NMDA) receptor, and it has a highin vivopotency as an excitotoxin. In fact, although QUIN has an uptake system, its neuronal degradation enzyme is rapidly saturated, and the rest of extracellular QUIN can continue stimulating the NMDA receptor. However, its toxicity cannot be fully explained by its activation of NMDA receptors it is likely that additional mechanisms may also be involved. In this review we describe 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.

Sign in / Sign up

Export Citation Format

Share Document