Kynurenine pathway enzymes in a rat model of chronic epilepsy: Immunohistochemical study of activated glial cells
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Regulation of NAD biosynthetic enzymes modulates NAD-sensing processes to shape mammalian cell physiology under varying biological cues
2015, Biochimica et Biophysica Acta - Proteins and ProteomicsCitation Excerpt :Due to the neurotoxic nature of the QA substrate, several studies have investigated the possible enzyme's involvement in the pathogenesis of neurodegenerative disorders characterized by a significant accumulation of QA deriving from KP activation. The increase of the enzyme activity in the brain of patients with Huntington disease [158] and with olivopontocerebellar atrophy [159], the increase of the enzyme level in glial cells of rat models of chronic epilepsy [160] and the increase of mRNA expression in the brain of Alzheimer disease mice [161] appear to suggest a neuroprotective function of the enzyme. However, it is evident that QAPRT activity is not sufficient to fulfill the role of QA scavenger.
Post-exposure administration of diazepam combined with soluble epoxide hydrolase inhibition stops seizures and modulates neuroinflammation in a murine model of acute TETS intoxication
2014, Toxicology and Applied PharmacologyCitation Excerpt :Electroconvulsive seizures (Steward, 1994) and kindled seizures (Steward et al., 1992) as well as organophosphate nerve agent-induced seizures (Baille-Le Crom et al., 1995; Baille et al., 2005; Liu et al., 2012; Zimmer et al., 1997) and kainic acid-induced SE (Drexel et al., 2012; Ravizza et al., 2005; Rizzi et al., 2003) are associated with reactive astrogliosis. Prolonged seizures have also been shown to rapidly activate microglia (Baille et al., 2005; Du et al., 1993; Rizzi et al., 2003; Zimmer et al., 1997). Based on data collected in these seizure models, it is postulated that the neuroinflammatory response is a consequence of neurodegeneration, and that the extent or severity of neurodegeneration and neuroinflammation is directly correlated to the duration and/or intensity of seizure activity (Drexel et al., 2012; McDonough et al., 1995, 1998; Shih et al., 2003).
Protective activity of α-lactoalbumin (ALAC), a whey protein rich in tryptophan, in rodent models of epileptogenesis
2012, NeuroscienceCitation Excerpt :The mechanism by which ALAC prevents full development of epileptic activity probably involves an increased delivery of TRP to the brain, with possible consequent enhancement of cerebral 5-HT synthesis and transmission (Citraro et al., 2011). An alternative speculative explanation could relate to the observation that TRP, in addition to acting as a 5-HT precursor, can be converted by cerebral indoleamine 2,3-dioxygenase to kynurenine (Du et al., 1993) and then to kynurenic acid, which acts as an NMDA receptor antagonist. However, laboratory analyses are needed in order to confirm the increase in both 5-HT and kynurenic acid.
Characterization of the convulsant action of pregnenolone sulfate
2004, Neuropharmacology