Hypolocomotion in rats with chronic liver failure is due to increased glutamate and activation of metabotropic glutamate receptors in substantia nigra

Cauli, Omar; Llansola, Marta; Erceg, Slaven; Felipo, Vicente

doi:10.1016/j.jhep.2006.06.019

Cited by 56 publications

(46 citation statements)

References 37 publications

(30 reference statements)

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“…Impairment of cognitive and motor functions has also been reported in hyperammonemic rats after portocaval anastomosis (PCA) and PVL [2]. In portocaval-shunted rats altered thalamo-cortical neurotransmission leading to hypokinesia is mediated by increased extracellular glutamate levels [3,4].…”

Section: Introductionmentioning

confidence: 99%

Locomotor impairment and cerebrocortical oxidative stress in portal vein ligated rats in vivo

Bruck

Görg

Bidmon

et al. 2011

Journal of Hepatology

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Section: Introductionmentioning

confidence: 99%

Locomotor impairment and cerebrocortical oxidative stress in portal vein ligated rats in vivo

Bruck

Görg

Bidmon

et al. 2011

Journal of Hepatology

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“…It has been well established for several decades that hyperammonemia leads to reduced glutamate uptake, which is caused by a reduced amount and function of glutamate transporters [26][27][28] . Moreover, it has been shown recently that reduced glutamate transporters and increased extracellular glutamate are responsible for hypokinesia in rats with HE and hyperammonemia [29] . GS plays a central role in the metabolic regulation of the excitatory neurotransmitter glutamate and in the detoxification of ammonia.…”

Section: Discussionmentioning

confidence: 99%

Glutamine synthetase activity and glutamate uptake in hippocampus and frontal cortex in portal hypertensive rats

Acosta¹,

Fernández²,

Roselló³

et al. 2009

WJG

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AIM:To study glutamine synthetase (GS) activity and glutamate uptake in the hippocampus and frontal cortex (FC) from rats with prehepatic portal vein hypertension. METHODS:Male Wistar rats were divided into shamoperated group and a portal hypertension (PH) group with a regulated stricture of the portal vein. Animals were sacrificed by decapitation 14 d after portal vein stricture. GS activity was determined in the hippocampus and FC. Specific uptake of radiolabeled L-glutamate was studied using synaptosome-enriched fractions that were freshly prepared from both brain areas. RESULTS:We observed that the activity of GS increased in the hippocampus of PH rats, as compared to control animals, and decreased in the FC. A significant decrease in glutamate uptake was found in both brain areas, and was more marked in the hippocampus. The decrease in glutamate uptake might have been caused by a deficient transport function, significantly and persistent increase in this excitatory neurotransmitter activity. CONCLUSION:The presence of moderate ammonia blood levels may add to the toxicity of excitotoxic glutamate in the brain, which causes alterations in brain function. Portal vein stricture that causes portal hypertension modifies the normal function in some brain regions.

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“…Abnormal movements, including psychomotor slowing and hypokinesia, may be part of the clinical spectrum of HE in its chronic form (Cauli et al 2006;Pomier-Layrargues 2001). Approximately 20-50% of patients with chronic liver failure have moderate to severe parkinsonism (Olanow 2004).…”

Section: Hepatic Encephalopathymentioning

confidence: 99%

Manganese accumulation in the CNS and associated pathologies

2011

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Manganese (Mn) is an essential metal for life. It is a key constituent of clue enzymes in the central nervous system, contributing to antioxidant defenses, energetic metabolism, ammonia detoxification, among other important functions. Until now, Mn transport mechanisms are partially understood; however, it is known that it shares some mechanisms of transport with iron. CNS is susceptible to Mn toxicity because it possesses mechanisms that allow Mn entry and favor its accumulation. Cases of occupational Mn exposure have been extensively reported in the literature; however, there are other ways of exposure, such as long-term parental nutrition and liver failure. Manganism and hepatic encephalopathy are the most common pathologies associated with the effects of Mn exposure. Both pathologies are associated with motor and psychiatric disturbances, related in turn to mechanisms of damage such as oxidative stress and neurotransmitters alterations, the dopaminergic system being one of the most affected. Although manganism and Parkinson's disease share some characteristics, they differ in many aspects that are discussed here. The mechanisms for Mn transport and its participation in manganism and hepatic encephalopathy are also considered in this review. It is necessary to find an effective therapeutic strategy to decrease Mn levels in exposed individuals and to treat Mn long term effects. In the case of patients with chronic liver failure it would be worthwhile to test a low-Mn diet in order to ameliorate symptoms of hepatic encephalopathy possibly related to Mn accumulation.

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Hypolocomotion in rats with chronic liver failure is due to increased glutamate and activation of metabotropic glutamate receptors in substantia nigra

Cited by 56 publications

References 37 publications

Locomotor impairment and cerebrocortical oxidative stress in portal vein ligated rats in vivo

Locomotor impairment and cerebrocortical oxidative stress in portal vein ligated rats in vivo

Glutamine synthetase activity and glutamate uptake in hippocampus and frontal cortex in portal hypertensive rats

Manganese accumulation in the CNS and associated pathologies

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