Excitatory amino acid release and electrocortical brain activity after hypoxemia in near-term lambs

Os, Sandra van; Ruitenbeek, W.; Hopman, J.C.W.; Bor, Margot van de

doi:10.1016/j.braindev.2005.12.002

Cited by 6 publications

(1 citation statement)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Under hypoxic conditions the disruption of the functional group of neurons that regulate the level of excitability of cortical neurons is one of the mechanisms of the development of pathological activity on the electro encephalo gramme (EEG) [22]. At the same time, it has been noticed, that based on a comparative analysis [23][24][25], it can be stated that the changes in the activity of the developing neurons under hypoxia lie in the same mechanisms that are typical for mature people. There are only some distinctive features [26,27]].…”

Section: Resultsmentioning

confidence: 99%

Effect of Pre-/ Postnatal Hypoxia on Pyruvate Kinase in Rat Brain

Rashidova¹

2018

International Journal of Secondary Metabolite

View full text Add to dashboard Cite

The effect of hypoxic hypoxia on the pyruvate kinase (PK) activity in the brain structures of white rats during ontogenesis in a comparative aspect has been studied. A clear dependence could be established in the increase of PK activity from an oxygen deficient state, the age of animals, the studied structure of the brain and the prolonged effect of hypoxia. Prenatal exposure to hypoxia has shown that the PK activity is not restored to the control value level in postnatal development. After postnatal exposure to hypoxia with increasing age in animals, the PK activity gets more resistant to the effect of stress-factors. The data analysis indicates that the increasing exhaustion of energy resources necessary for normal cell functioning makes an important contribution to the development of hypoxic state and the insufficiency of mitochondrial oxidative phosphorylation, the main energy forming system which underlies these disturbances. Energy-shortage, in its turn causes a variety of secondary negative metabolic alterations and gives rise to free radical oxidation in the cells. An explanation of the obtained results suggested can be considered as an evidence of the realization of the biological effect of hypoxia through the oxidative mechanism.

show abstract

Section: Resultsmentioning

confidence: 99%

Effect of Pre-/ Postnatal Hypoxia on Pyruvate Kinase in Rat Brain

Rashidova¹

2018

International Journal of Secondary Metabolite

View full text Add to dashboard Cite

show abstract

Protective effect of selaginellin on glutamate-induced cytotoxicity and apoptosis in differentiated PC12 cells

Wang

et al. 2009

Naunyn-Schmied Arch Pharmacol

View full text Add to dashboard Cite

L-glutamate plays a key role in neuronal cell death associated with many neurodegenerative conditions such as cerebral ischemia, hypoxia, Alzheimer's, Huntington's, and Parkinson's diseases. Selaginellin, a component extracted from Saussurea pulvinata (Hook.et Grev.) Maximo, was assessed for its ability to protect rat pheochromocytoma (PC12) cells against oxidative toxicity induced by glutamate. The differentiated PC12 cells were pretreated with various concentrations (10(-7), 3 x 10(-7), or 10(-6) M) of selaginellin for 1 h prior to exposure to L-glutamate. Selaginellin was shown to protect PC12 cells against glutamate toxicity, as determined by characteristic morphological features, lactate dehydrogenase release and cell viability, and apoptosis as evaluated by Hoechst 33342 staining assay and caspase-3 activity. In addition, the increase in levels of reactive oxygen species and decrease in klotho gene expression induced by glutamate were significantly reversed by selaginellin. Our study suggests that selaginellin has a neuroprotective effect against L-glutamate-induced neurotoxicity through mechanisms related to anti-oxidation and anti-apoptosis via scavenging reactive oxygen species and up-regulating the expression of klotho gene.

show abstract