Cerebrospinal fluid hypoxanthine, xanthine and uric acid levels may reflect glutamate-mediated excitotoxicity in different neurological diseases
References (22)
- et al.
Oxygen free radicals regulate NMDA receptor function via a redox modulatory site
Neuron
(1990) - et al.
Blockade of N-methyl-d-aspartate-sensitive acidic amino acid receptors inhibits ischemia-induced accumulation of purine catabolites in the rat striatum
Neurosci. Lett.
(1986) - et al.
Allopurinol inhibits uric acid accumulation in the rat brain following focal cerebral ischemia
Brain Res.
(1989) - et al.
Glutamate becomes neurotoxic via the N-methyl-d-aspartate receptor when intracellular energy levels are reduced
Brain Res.
(1988) - et al.
Ultrastructural immunocytochemical observations on the localization, metabolism and transport of glutamate in normal and ischemic brain tissue
Prog. Brain Res.
(1992) Identification of hypoxanthine transport and xanthine oxidase activity in brain capillaries
J. Neurochem.
(1985)- et al.
Differential distribution of purine metabolizing enzymes between glia and neurons
J. Neurochem.
(1994) - et al.
Oxidative stress, glutamate, and neurodegenerative disorders
Science
(1993) - et al.
Relationships among ATP synthesis, K+ gradients, and neurotransmitter amino acid levels in isolated rat brain synaptosomes
J. Neurochem.
(1987) - et al.
Patterns of increased glucose use following extracellular infusion of glutamate: an autoradiographic study
J. Neurotrauma
(1996)
Evidence for differential function of neuronal and glial cells in protein metabolism and amino acid transport
J. Neurosci. Res.
Cited by (89)
A novel approach with glass needle enclosed movable probe for in vivo real-time detection of glucose in cisternal cerebrospinal fluid
2020, Journal of Electroanalytical ChemistryCitation Excerpt :As shown in Fig. 2A, the present probe exhibited strong response towards glucose (1 mM), whereas no signal or only slight response was observed towards AA (200 μM), UA (20 μM) or DA (1 μM). The tested concentrations of the interferents were chosen based on their physiological levels [25–29]. Thereafter, the response to glucose (1 mM) was still significant.
Aberrant energy metabolism and redox balance in seizure onset zones of epileptic patients
2020, Journal of ProteomicsThe value of serum uric acid levels to differentiate causes of transient loss of consciousness
2019, Epilepsy and BehaviorCitation Excerpt :Previous studies have suggested [6,10,11] that seizures can cause an increase in uric acid production in the body, leading to elevated serum uric acid levels. While other investigations have reported elevated levels of uric acid in the cerebrospinal fluid of patients with epilepsy [12]. Animal experiments [13,14] have also revealed elevated levels of uric acid in the brain during episodes of seizures.
<sup>1</sup>H NMR metabolic signature of cerebrospinal fluid following repetitive lower-limb remote ischemia preconditioning
2018, Neurochemistry InternationalUric acid and allopurinol aggravate absence epileptic activity in Wistar Albino Glaxo Rijswijk rats
2018, Brain ResearchCitation Excerpt :Indeed, it has been demonstrated that uric acid itself has direct proinflammatory effects (Kanellis et al., 2003). Thus, it is possible that uric acid exerts its effects on several diseases, such as absence epilepsy by activation of inflammatory processes when its level is increased (Layton et al., 1998; Lühdorf et al., 1978; Oses et al., 2007; Stover et al., 1997; Thyrion et al., 2016a): uric acid can trigger inflammatory responses (e.g., enhances caspase-1 activity), which increase, among others, the level of the IL-1β, and elevates cortical excitability through interleukin-1 receptor (IL-1R)/COX-2/prostaglandin E2 (PGE2) system (Vezzani et al., 2011). These effects may shift the excitatory/inhibitory balance to the excitation in the somatosensory cortex (cortical focus of absence epilepsy genesis), which hyperexcitability may increase the number of SWDs in WAG/Rij rats (Coenen and Van Luijtelaar, 2003; Kovács et al., 2006, 2011a, 2014; Van Luijtelaar et al., 2012).
Fatigue in multiple sclerosis – Insights into evaluation and management
2017, Neurophysiologie Clinique