Characterization of cellular and neurological damage following unilateral hypoxia/ischemia

Olson, Ellen; McKeon, Robert J.

doi:10.1016/j.jns.2004.07.021

Cited by 53 publications

(28 citation statements)

References 33 publications

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“…In our piglets, via 2DE, GFAP was identified as increased after IHH. This is in agreement with many other reports describing increased expression of GFAP in response to hypoxia in the hippocampus of different species and at different developmental ages [30,31]. Similar to 14-3-3h/s above, WB did not support the 2DE findings for GFAP.…”

Section: Discussionsupporting

confidence: 87%

Intermittent Hypercapnic Hypoxia Induced Protein Changes in the Piglet Hippocampus Identified by MALDI-TOF-MS

et al. 2009

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Intermittent hypercapnic hypoxia (IHH) induces protein changes in the brainstem, but its effects on the hippocampus have not yet been studied. Using a proteomics-based approach, we tested the hypothesis that IHH up-regulates apoptotic promoters and down-regulates apoptotic inhibitors in the developing hippocampus. Male piglets aged 13-14 days were assigned to control (n = 6) or IHH (n = 5) groups. Using two-dimensional polyacrylamide gel electrophoresis, matrix-assisted laser desorption/ionisation-time of flight-mass spectrometry (MALDI-TOF-MS), a total of 26 protein spots were differentially expressed in IHH compared to control group. Thirteen of these (6 up-regulated, 7 down-regulated) were identified including 14-3-3θ/τ (increased), glial fibrillary acidic protein (increased) and a-internexin (decreased). Further analysis with western blot validated these proteins and immunohistochemistry showed specific regional changes in the subiculum, stratum radiatum and CA1 of the hippocampus. Most proteins identified were involved in promoting cell survival under apoptotic conditions. These findings improve our understanding of the cellular processes that occur in the hippocampus during IHH exposure, and have important implications in clinical settings where IHH is experienced, for example, during prone sleeping or with obstructive sleep apnea in an infant.

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Section: Discussionsupporting

confidence: 87%

Intermittent Hypercapnic Hypoxia Induced Protein Changes in the Piglet Hippocampus Identified by MALDI-TOF-MS

et al. 2009

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“…Interestingly, the learning-responding IR gene expression showed a regional specificity with a persistent up-regulation only in the CA1 region, similar to our previous findings (Zhao et al 1999), and a profound down-regulation in the CA3 region. Although the precise roles of the CA1 and the CA3 region in Cold Spring Harbor Laboratory Press on May 11, 2018 -Published by learnmem.cshlp.org Downloaded from memory processing are not yet fully understood, the CA1 neurons have been shown to be the most reactive cells in response to both physiological input such as learning (Frank et al 2004;Knafo et al 2004;Nolan et al 2004) and pathological stimuli such as ischemia, hypoxia (Lukyanetz et al 2003;Englund et al 2004;Olson and McKeon 2004), and hyperglycemia (the present study). It is not surprising, therefore, that CA1 neurons are equipped with active signal transduction systems including those regulated by tyrosine receptor kinases such as the insulin receptor.…”

Section: Discussionmentioning

confidence: 63%

Insulin receptor signaling in long-term memory consolidation following spatial learning

Dou¹,

Chen²,

Dufour³

et al. 2005

Learn. Mem.

189

142

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Evidence has shown that the insulin and insulin receptor (IR) play a role in cognitive function. However, the detailed mechanisms underlying insulin's action on learning and memory are not yet understood. Here we investigated changes in long-term memory-associated expression of the IR and downstream molecules in the rat hippocampus. After long-term memory consolidation following a water maze learning experience, gene expression of IR showed an up-regulation in the CA1, but a down-regulation in the CA3 region. These were correlated with a significant reduction in hippocampal IR protein levels. Learning-specific increases in levels of downstream molecules such as IRS-1 and Akt were detected in the synaptic membrane accompanied by decreases in Akt phosphorylation. Translocation of Shc protein to the synaptic membrane and activation of Erk1/2 were also observed after long-term memory formation. Despite the clear memory-correlated alterations in IR signaling pathways, insulin deficits in experimental diabetes mellitus (DM) rats induced by intraperitoneal injections of streptozotocin resulted in only minor memory impairments. This may be due to higher glucose levels in the DM brain, and to compensatory mechanisms from other signaling pathways such as the insulin-like growth factor-1 receptor (IGF-1R) system. Our results suggest that insulin/IR signaling plays a modulatory role in learning and memory processing, which may be compensated for by alternative pathways in the brain when an insulin deficit occurs.Insulin/insulin receptor plays diverse roles in brain functions including learning and memory. Cognition-enhancing effects of insulin have been reported in both human and animal experiments (Kern et al. 1999(Kern et al. , 2001Park et al. 2000), whereas impairments in insulin and the brain insulin receptor (IR) have been linked to development of aging-associated brain degenerative disorders such as Alzheimer's disease (Craft et al. 1996;Frolich et al. 1998;Gasparini and Xu 2003;Watson and Craft 2003). Unlike its peripheral counterpart, insulin/insulin receptor in the brain does not appear to exert a direct effect on neuronal glucose metabolism, but most likely plays a modulatory role, via activating specific signal transduction cascades, in synaptic activities involved in memory formation. Evidence has shown that insulin/ insulin receptor is involved in regulation of neurotransmitter release (Bhattacharya and Saraswati 1991;Figlewicz and Szot 1991), receptor conductance and trafficking (Wan et al. 1997;Beattie et al. 2000;Lin et al. 2000;Man et al. 2000;Skeberdis et al. 2001;Zhou et al. 2001), and intracellular Ca 2+ release and neuropeptide secretion (Jonas et al. 1997). As a receptor tyrosine kinase, the insulin receptor in the hippocampus was shown to respond to learning experiences by alterations in its gene expression and activation of downstream molecules such as Shc/Erk1/2 in an early stage of memory formation (Zhao et al. 1999).Despite the accumulated evidence, contradictory results appear to exist regarding ...

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“…Conditions in which the brain temporarily becomes hypoxic, such as stroke, cardiac arrest, cardiovascular surgery and neurosurgical procedures, can cause death and disability (Olson & McKeon, 2004). Transient cerebral ischemia is induced by temporary deprivation of blood flow to the brain.…”

Section: Introductionmentioning

confidence: 99%

Comparison of neuroprotective effects of extract and fractions fromAgarum clathratumagainst experimentally induced transient cerebral ischemic damage

Kim

Yoo

Park

et al. 2013

Pharmaceutical Biology

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Objective: We investigated the neuroprotective effects of crude-extract, ethyl acetate (EA)-, n-butanol (BU)-, dichloromethane (DCM)-and n-hexane (Hx)-fractions from A. clathratum on ischemic damage in the gerbil hippocampal CA1 region (CA1) after 5 min of transient cerebral ischemia. Materials and methods: Agarum clathratum was collected in Kangwon province (South Korea) and treated with 95% ethanol. The ethanol extract was suspended in distilled water and subjected to a series of partitions with EA, BU, DCM and Hx. Each of extract and fraction was orally administered with 50 mg/kg once a day for one week before ischemia-reperfusion (I-R).Result: In the crude-extract-, EA-and BU-fraction-treated ischemia groups, we found strong neuroprotection in the CA1 -about 80-89% of CA1 pyramidal neurons survived. However, in the DCM-and Hx-fraction-treated ischemia groups, we did not find any significant neuroprotection. In addition, we observed changes in astrocytes and microglia in the ischemic CA1. In the crude-extract, EA-and BU-fraction-treated ischemia groups, the distribution pattern and activity of the glial cells were similar to that found in the sham group. Discussion: Repeated supplements of crude-extract, EA-and BU-fractions of A. clathratum could protect neurons from I-R injury in the hippocampal CA1 induced by transient cerebral ischemia via decrease of glial activation.

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Characterization of cellular and neurological damage following unilateral hypoxia/ischemia

Cited by 53 publications

References 33 publications

Intermittent Hypercapnic Hypoxia Induced Protein Changes in the Piglet Hippocampus Identified by MALDI-TOF-MS

Intermittent Hypercapnic Hypoxia Induced Protein Changes in the Piglet Hippocampus Identified by MALDI-TOF-MS

Insulin receptor signaling in long-term memory consolidation following spatial learning

Comparison of neuroprotective effects of extract and fractions fromAgarum clathratumagainst experimentally induced transient cerebral ischemic damage

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