Behavioral and electrophysiological correlates of the quinolinic acid rat model of Huntington's disease in rats

Popoli, Patrizia; Pézzola, Antonella; Domenici, Maria Rosaria; Sagratella, S.; Diana, Giovanni; Caporali, Maurizio; Bronzetti, Elena; Vega, J. A.; Carolis, A. Scotti de

doi:10.1016/0361-9230(94)90109-0

Cited by 35 publications

(19 citation statements)

References 43 publications

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“…In Huntington's disease brain, quinolinic acid is present in higher concentrations than controls Schwarcz 1999, Guidetti et al 2004), and in animals generates a model in which the behavioural, neurochemical and electrophysiological consequences closely mimic those seen in the human disease (Popoli et al 1994).…”

Section: Discussionmentioning

confidence: 95%

5-Hydroxyanthranilic Acid, a Tryptophan Metabolite, Generates Oxidative Stress and Neuronal Death via p38 Activation in Cultured Cerebellar Granule Neurones

Smith

Stone

2009

Neurotox Res

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The essential amino acid tryptophan is primarily metabolised through the kynurenine pathway, some components of which may be neurotoxic. We have now examined the potential toxicity of several kynurenine metabolites in relation to the generation of oxidative stress and activation of cell death signalling pathways in cultured cerebellar granule neurons. 3-Hydroxykynurenine (3HK), 3-hydroxyanthranilic acid (3HAA) and 5-hydroxyanthranilic acid (5HAA) induced cell death which increased with exposure time and compound concentration. The neurotoxic effects of 3HK, 3HAA and 5HAA were prevented by catalase, but not by superoxide dismutase. In addition, Western blot analysis demonstrated p38 activation due to 3HK or 5HAA treatment, although caspase-3 activation was not evident in either case. The results indicate that kynurenine metabolites can be neurotoxic via a caspase-3 independent mechanism, and that the minor metabolite 5HAA is as potent a toxin as the better documented compounds 3HK and 3HAA.

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Section: Discussionmentioning

confidence: 95%

5-Hydroxyanthranilic Acid, a Tryptophan Metabolite, Generates Oxidative Stress and Neuronal Death via p38 Activation in Cultured Cerebellar Granule Neurones

Smith

Stone

2009

Neurotox Res

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“…Quinolinic acid neurotoxicity is a possible mechanism by which learning is impaired in active avoidance; studies in which quinolinic acid was administered i.c.v. Similarly, Popoli et al (28) produced learning impairment in rats by administering quinolinic acid to the striatum 8 wk before testing animals in the Morris water maze. Similarly, Popoli et al (28) produced learning impairment in rats by administering quinolinic acid to the striatum 8 wk before testing animals in the Morris water maze.…”

Section: Discussionmentioning

confidence: 99%

“…showed that it impaired spatial learning in rats (25)(26)(27). Similarly, Popoli et al (28) produced learning impairment in rats by administering quinolinic acid to the striatum 8 wk before testing animals in the Morris water maze. Another possibility is that performance impairment in the active avoidance procedure is related to increased levels of platelet-activating factor (PAF) caused by LP-BM5 infection (20).…”

Section: Discussionmentioning

confidence: 99%

LP‐BM5 infection impairs acquisition, but not performance, of active avoidance responding in C57Bl/6 mice

1998

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LP-BM5 murine leukemia virus infection causes an AIDS-like syndrome--murine acquired immunodeficiency syndrome--in C57B1/6 mice and impairs spatial learning in the Morris water maze without gross motor impairment. We used a shuttle shock-avoidance procedure to examine the effects of LP-BM5 infection on learning and retention of avoidance behavior. Thirty mice were inoculated with LP-BM5; 30 received vehicle (DMEM) injections. Fifteen LP-BM5 and 15 DMEM mice were trained in avoidance 7 wk after inoculation; retention of the avoidance response was tested 4 wk later. The remaining mice were trained 11 wk after inoculation. In animals trained 7 wk after inoculation, the groups performed similarly, with a marginally significant tendency for LP-BM5-infected animals to make more avoidance responses. This group difference was significant when animals were retested at 11 wk. However, LP-BM5 animals trained 11 wk after inoculation made significantly fewer avoidance responses than controls trained at the same time. We conclude that in later stages of disease, LP-BM5 impairs response acquisition, but not performance, in the active avoidance procedure. Results extend the use of the LP-BM5-infected mouse as a model of AIDS dementia complex.

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“…TNF-␣, IL-1, and other cytokines induce astrocytosis [28]. Astrocytosis also is triggered by QUIN injections into the brain [51].…”

Section: Glial Fibrillary Acidic Proteinmentioning

confidence: 99%

The SIV-infected rhesus monkey model for HIV-associated dementia and implications for neurological diseases

Rausch

Murray

Eiden

1999

Journal of Leukocyte Biology

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Behavioral and electrophysiological correlates of the quinolinic acid rat model of Huntington's disease in rats

Cited by 35 publications

References 43 publications

5-Hydroxyanthranilic Acid, a Tryptophan Metabolite, Generates Oxidative Stress and Neuronal Death via p38 Activation in Cultured Cerebellar Granule Neurones

5-Hydroxyanthranilic Acid, a Tryptophan Metabolite, Generates Oxidative Stress and Neuronal Death via p38 Activation in Cultured Cerebellar Granule Neurones

LP‐BM5 infection impairs acquisition, but not performance, of active avoidance responding in C57Bl/6 mice

The SIV-infected rhesus monkey model for HIV-associated dementia and implications for neurological diseases

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