Neonatal hypoxia–ischemia reduces ganglioside, phospholipid and cholesterol contents in the rat hippocampus

Ramirez, Maria Rosana; Muraro, Francine; Zylbersztejn, Daniel Suslik; Abel, Cristiano R.; Arteni, Nice Sarmento; Lavinsky, Daniel; Netto, Carlos Alexandre; Trindade, Vera Maria Treis

doi:10.1016/s0168-0102(03)00100-7

Cited by 28 publications

(19 citation statements)

References 63 publications

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“…During prolonged hypoxia, the mitochondria in the majority of neonatal neurons were slowly depolarized, and during a brief period of hypoxia followed by reoxygenation, the majority of the neonatal mitochondria demonstrated a partial depolarization followed by recovery, which correlates with the previous studies (41). In the study of mitochondrial integrity, we observed a decrease in the percentage of positive cells to NAO in the HI group in the first hours in the brainstem, which supports the idea that the oxidation of cardiolipin is implicated in mitochondrial dysfunction and can be the consequence of release of cytochrome C from the mitochondria to the cytoplasm, a process that is involved in the apoptotic cell death cascade (16,17,19,55). Moreover, the same results were found in the percentage of positive cells to Rhodamine 123, suggesting that both membrane potential and integrity are altered during the HI event in the first moments.…”

Section: Discussionsupporting

confidence: 90%

Antioxidant Treatments Recover the Alteration of Auditory‐Evoked Potentials and Reduce Morphological Damage in the Inferior Colliculus after Perinatal Asphyxia in Rat

et al. 2015

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Maturation of the auditory pathway is dependent on the central nervous system myelination and it can be affected by pathologies such as neonatal hypoxic ischemic (HI) encephalopathy. Our aim was to evaluate the functional integrity of the auditory pathway and to visualize, by histological and cellular methods, the damage to the brainstem using a neonatal rat model of HI brain injury. To carry out this morphofunctional evaluation, we studied the effects of the administration of the antioxidants nicotine, melatonin, resveratrol and docosahexaenoic acid after hypoxia-ischemia on the inferior colliculus and the auditory pathway. We found that the integrity of the auditory pathway in the brainstem was altered as a consequence of the HI insult. Thus, the auditory brainstem response (ABR) showed increased I-V and III-V wave latencies. At a histological level, HI altered the morphology of the inferior colliculus neurons, astrocytes and oligodendricytes, and at a molecular level, the mitochondria membrane potential and integrity was altered during the first hours after the HI and reactive oxygen species (ROS) activity is increased 12 h after the injury in the brainstem. Following antioxidant treatment, ABR interpeak latency intervals were restored and the body and brain weight was recovered as well as the morphology of the inferior colliculus that was similar to the control group. Our results support the hypothesis that antioxidant treatments have a protective effect on the functional changes of the auditory pathway and on the morphological damage which occurs after HI insult.

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Section: Discussionsupporting

confidence: 90%

Antioxidant Treatments Recover the Alteration of Auditory‐Evoked Potentials and Reduce Morphological Damage in the Inferior Colliculus after Perinatal Asphyxia in Rat

et al. 2015

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“…It is suggested that hypoxia could have activated neuraminidase and change directly the content of ganglioside-bound sialic acid on the synaptic plasma membrane. Neonatal hypoxia/ischemia is reported to reduce ganglioside content in the rat hippocampus (14). In contrast to the above studies, we explored the effect of sodium nitrite-induced hypoxia on glycolipids at brain subcellular level and our findings demonstrate an increase in the glycolipid content in the nuclear fraction.…”

Section: Resultsmentioning

confidence: 88%

“…It is supposed that gangliosides may promote neuronal regeneration through modulation of trophic factors (14,18). The high content of cerebrosides after hypoxia makes the membranes steadier and it appears to be a protective and compensatory mechanism against hypoxic damage.…”

Section: Resultsmentioning

confidence: 99%

Glycolipid Content of the Nuclear Membrane in Hypoxic Rat Brain

Petrova

Dishkelov

Vasileva

et al. 2012

Biotechnology & Biotechnological Equipment

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“…In mutant mice lacking GM1 and GD1a in the CNS, some paranodal oligodendrocyte loops failed to attach to the axolemma to form myelin sheaths, the expression of Caspr and NF155 was reduced, and the content of these proteins in lipid rafts was also reduced (7). A significant reduction of several gangliosides was observed after HI (21), which may contribute to the structural changes in the myelin sheaths. In our study, we found that HI led to a decrease of GM1 and NF155 in lipid rafts, suggesting that during the perinatal stage HI may destroy the structure of lipid rafts, change the lipid and protein composition of lipid rafts in paranodes, decrease paranodal junction stability, and induce abnormal myelin development.…”

Section: Discussionmentioning

confidence: 99%

GM1 improves neurofascin155 association with lipid rafts and prevents rat brain myelin injury after hypoxia-ischemia

Zhang

Huang

Zhao

et al. 2011

Braz J Med Biol Res

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White matter injury characterized by damage to myelin is an important process in hypoxic-ischemic brain damage (HIBD). Because the oligodendrocyte-specific isoform of neurofascin, neurofascin 155 (NF155), and its association with lipid rafts are essential for the establishment and stabilization of the paranodal junction, which is required for tight interaction between myelin and axons, we analyzed the effect of monosialotetrahexosyl ganglioside (GM1) on NF155 expression and its association with lipid rafts after HIBD in Sprague-Dawley rats, weighing 12-15 g, on day 7 post-partum (P7; N = 20 per group). HIBD was induced on P7 and the rats were divided into two groups: one group received an intraperitoneal injection of 50 mg/kg GM1 three times and the other group an injection of saline. There was also a group of 20 sham-operated rats. After sacrifice, the brains of the rats were removed on P30 and studied by immunochemistry, SDS-PAGE, Western blot analysis, and electron microscopy. Staining showed that the saline group had definite rarefaction and fragmentation of brain myelin sheaths, whereas the GM1 group had no obvious structural changes. The GM1 group had 1.9-2.9-fold more GM1 in lipid rafts than the saline group (fraction 3-6; all P < 0.05) and 0.5-2.4-fold higher expression of NF155 in lipid rafts (fraction 3-5; all P < 0.05). Injection of GM1 increased the content of GM1 in lipid rafts as well as NF155 expression and its lipid raft association in HIBD rat brains. GM1 may repair the structure of lipid rafts, promote the association of NF155 (or other important proteins) with lipid rafts, stabilize the structure of paranodes, and eventually prevent myelin sheath damage, suggesting a novel mechanism for its neuroprotective properties.

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Neonatal hypoxia–ischemia reduces ganglioside, phospholipid and cholesterol contents in the rat hippocampus

Cited by 28 publications

References 63 publications

Antioxidant Treatments Recover the Alteration of Auditory‐Evoked Potentials and Reduce Morphological Damage in the Inferior Colliculus after Perinatal Asphyxia in Rat

Antioxidant Treatments Recover the Alteration of Auditory‐Evoked Potentials and Reduce Morphological Damage in the Inferior Colliculus after Perinatal Asphyxia in Rat

Glycolipid Content of the Nuclear Membrane in Hypoxic Rat Brain

GM1 improves neurofascin155 association with lipid rafts and prevents rat brain myelin injury after hypoxia-ischemia

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