Neuronal death and tumor necrosis factor-α response to glutamate-induced excitotoxicity in the cerebral cortex of neonatal rats

Chaparro-Huerta, V.; Rivera-Cervantes, M.C.; Torres-Mendoza, Blanca Miriam; Beas‐Zárate, Carlos

doi:10.1016/s0304-3940(02)01006-6

Cited by 41 publications

(29 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Although detailed mapping of lesioned neurons following neonatal MSG treatment is not available, it is known that besides the retina and the arcuate nucleus, several other brain areas show neuronal degeneration and/or neurochemical changes due to the toxic effects of MSG (Olney, 1969;Frieder and Grimm, 1987;Gonzalez-Burgos et al, 2001;Beas-Zarate et al,. 2002;Chaparro-Huerta et al, 2002). Therefore, the observed changes in the neurobehavioral development may be partly due to the toxic effects of MSG in neurons responsible for normal motor development.…”

Section: Discussionmentioning

confidence: 99%

“…Although neonatal MSG treatment causes cell loss, morphological and biochemical alterations in various brain areas (Seress et al, 1984;van Rijn et al, 1986;Kubo et al, 1993;Ishikawa et al, 1997;Gonzalez-Burgos et al, 2001;Beas-Zarate et al, 2002;Chaparro-Huerta et al, 2002;Pesini et al,. 2004;Stricker-Krongrad and Beck, 2004;Tamas et al, 2004;), the most well-established morphological effect of neonatal MSG-treatment is the destruction of the neurons in the arcuate nucleus (Olney, 1969;Arees and Mayer, 1970;Heiman and Ben-Jonathan, 1983).…”

Section: Histological Analysismentioning

confidence: 99%

“…However, administration of MSG to neonatal rodents brings about several profound changes. It leads to degeneration of the neurons in the arcuate nucleus, inner retinal layers and various other brain areas (Olney, 1969;Arees and Mayer, 1970;Heiman and Ben-Jonathan, 1983;van Rijn et al, 1986;Kubo et al, 1993;Ishikawa et al, 1997;Gonzalez-Burgos et al, 2001;Beas-Zarate et al, 2002;Chaparro-Huerta et al, 2002;Pesini et al,. 2004;Stricker-Krongrad and Beck, 2004;Tamas et al, 2004), along with endocrinological, neurochemical and circadian alterations (Lengvari, 1977;Dawson and Lorden, 1981;Miyabo et al, 1985;Mistlberger and Antle, 1999;Schoelch et al, 2002;Urena-Guerrero et al, 2003;Kim et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Development of neurological reflexes and motor coordination in rats neonatally treated with monosodium glutamate

et al. 2005

View full text Add to dashboard Cite

Monosodium glutamate (MSG) treatment of neonatal rats causes neuronal degeneration in various brain areas and leads to several neurochemical, endocrinological and behavioral alterations. However, relatively little is known about the development of neurological reflexes and motor coordination of these animals. Therefore, the aim of the present study was to examine the neurobehavioral development of newborn rats treated with MSG. Rats received MSG at postnatal days 1, 3, 5, 7, and 9. Appearance of neural reflexes and reflex performance as well as motor coordination were examined for 5 weeks after birth. The efficacy of MSG treatment was confirmed by histological examination of the arcuate nucleus. We found that MSG treatment delayed the appearance of forelimb placing, forelimb grasp and righting reflexes, besides the retarded somatic development. The treated pups performed surface righting in significantly longer times. Also, worse performance was observed in the foot-fault and rota-rod tests. However, MSG-treated rats reached control levels by the end of the fifth postnatal week. These results show that MSG treatment does not cause permanent alterations in the neurobehavioral development, only delays the appearance of some reflexes and leads to temporary changes in reflex performance and motor coordination signs.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Histological Analysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Development of neurological reflexes and motor coordination in rats neonatally treated with monosodium glutamate

et al. 2005

View full text Add to dashboard Cite

show abstract

“…Glutamate in high doses produced neuroendocrine abnormalities (Moreno et al, 2005), neurodegeneration, neurotoxicity (Chapano-Hue et al, 2002), and oxidative damage in different organs (Farombi & Onyema, 2006;Pavlovic et al, 2007). Glutamate receptors known as mGluRI were strongly suggestive of the initiation of an epileptogenic process, one in which normal neuronal cortex is converted into a persistently hyperexcise state with a lowered threshold for the production of seizure discharges.…”

Section: Discussionmentioning

confidence: 99%

Alteration of pentylenetetrazole-induced seizure threshold by chronic administration of ginger (Zingiber officinale) extract in male mice

Hosseini

Mirazi

2015

Pharmaceutical Biology

View full text Add to dashboard Cite

Context: Zingiber officinale Roscoe (Zingiberaceae), or ginger, used in traditional Chinese medicine, has antioxidant activity and neuroprotective effects. The effects of this plant on clonic seizure have not yet been studied. Objective: The present study evaluated the anticonvulsant effect of ginger in a model of clonic seizures induced with pentylenetetrazole (PTZ) in male mice. Materials and methods: The anticonvulsant effect of Z. officinale was investigated using i.v. PTZ-induced seizure models in mice. Different doses of the hydroethanolic extract of Z. officinale (25, 50, and 100 mg/kg) were administered intraperitonal (i.p.), daily for 1 week before induction of PTZ. Phenobarbital sodium (30 mg/kg), a reference standard, was also tested for comparison. The effect of ginger on to the appearance of three separate seizure endpoints, e.g., myoclonic, generalized clonic, and tonic extension phase, was recorded. Results: Hydroethanolic extract of Z. officinale significantly increased the onset time of myoclonic seizure at doses of 25-100 mg/kg (55.33 ± 1.91 versus 24.47 ± 1.33 mg/kg, p50.001) and significantly prevented generalized clonic (74.64 ± 3.52 versus 47.72 ± 2.31 mg/kg, p50.001) and increased the threshold for the forelimb tonic extension (102.6 ± 5.39 versus 71.82 ± 7.82 mg/kg, p50.01) seizure induced by PTZ compared with the control group. Discussion and conclusion: Based on the results, the hydroethanolic extract of ginger has anticonvulsant effects, possibly through an interaction with inhibitory and excitatory systems, antioxidant mechanisms, and oxidative stress inhibition. KeywordsAnticonvulsant effect, antioxidant activity, clonic seizure, forelimb/hindlimbs tonic extension, neuroprotective effect, PTZ-induced seizure, traditional Chinese medicine History

show abstract

“…Specifically, IL-1 β stimulates glutamate uptake in glial cells by accelerating membrane trafficking of Na + /K + -ATPase via actin depolymerization [26], whereas TNF potentiates glutamate neurotoxicity by inhibiting glutamate uptake [27] or releases glutamate from hemi-channels of activated microglia in an autocrine manner [28]. Both IL-1β and TNF-α induce glutaminase expression, associated with an intracellular and extracellular increased concentrations of glutamate and with neuronal death via an apoptosislike mechanism, which selectively targets neurons expressing glutamate receptors [29][30][31]. Finally, the activation of the Ca 2+ permeable NMDA receptor alters the mitochondrial potential, causing membrane depolarization, affecting the mitochondrial electron transport linked to cytochrome c releasing [32].…”

Section: Neuroinflammation Oxidative Stress and Excitotoxicity In Nementioning

confidence: 99%

Cannabinoids in Neuroinflammation, Oxidative Stress and Neuro Excitotoxicity

M¹

2015

Pharm Anal Acta

View full text Add to dashboard Cite

Research on cannabinoids has been growing significantly in the last five years. More than fifty percent of this research corresponds to "cannabinoids and brain", particularly about neurodegeneration. In this sense, there is evidence reporting that specific phyto cannabinoids show some specific action on each one of main pathogenic mechanisms involved in neurodegeneration such as oxidative stress, neuroinflammation and excitotoxicity. However, by using the same targets, cannabinoids may also induce the opposite effects, this is, excitotoxicity and inflammation. In fact, both tetrahydro cannabinol and cannabidiol activate cannabinoid receptors, but they also may act as antagonists of those receptors. It seems to be a dose-dependent issue; nonetheless, as reviewed in this paper, many other factors such as timing, type of cell and its state of activity even the activation of different, noncannabinoid receptorsseem to have a role related to those unexpected antagonic effects.

show abstract

Neuronal death and tumor necrosis factor-α response to glutamate-induced excitotoxicity in the cerebral cortex of neonatal rats

Cited by 41 publications

References 22 publications

Development of neurological reflexes and motor coordination in rats neonatally treated with monosodium glutamate

Development of neurological reflexes and motor coordination in rats neonatally treated with monosodium glutamate

Alteration of pentylenetetrazole-induced seizure threshold by chronic administration of ginger (Zingiber officinale) extract in male mice

Cannabinoids in Neuroinflammation, Oxidative Stress and Neuro Excitotoxicity

Contact Info

Product

Resources

About