Effect of protein kinases on lactate dehydrogenase activity in cortical neurons during hypoxia

Hong, Soon‐Sun; Gibney, Geoffrey T.; Esquilin, Manny; Yu, J.B.; Xia, Ying

doi:10.1016/j.brainres.2004.03.004

Cited by 26 publications

(17 citation statements)

References 24 publications

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“…Although V-wave assessment is less unsettling/painful than transcranial or cervicomedular stimulation techniques (McNeil et al 2013), V-waves have been used only rarely to investigate exercise-induced fatigue (Racinais et al 2007) and never under hypoxic conditions. Hypoxia is, however, known to impair in vitro CNS function (cerebral neuron excitability, ion channels, signaling pathways, synaptic neurotransmission) (Cater et al 2003;Hong et al 2004;Lopez-Barneo et al 2001), and evidence demonstrating that hypoxiainduced cerebral perturbations strongly contribute to exercise performance limitation are growing (Amann et al 2006;Peltonen et al 1997) despite conflicting results in studies that investigated in vivo corticospinal excitability (for a review see Verges et al 2012).…”

Section: Introductionmentioning

confidence: 98%

Modulation of exercise-induced spinal loop properties in response to oxygen availability

et al. 2014

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This study investigated the effects of acute hypoxia on spinal reflexes and soleus muscle function after a sustained contraction of the plantar flexors at 40% of maximal voluntary isometric contraction (MVC). Fifteen males (age 25.3 ± 0.9 year) performed the fatigue task at two different inspired O₂ fractions (FiO₂ = 0.21/0.11) in a randomized and single-blind fashion. Before, at task failure and after 6, 12 and 18 min of passive recovery, the Hoffman-reflex (H max) and M-wave (M max) were recorded at rest and voluntary activation (VA), surface electromyogram (RMSmax), M-wave (M sup) and V-wave (V sup) were recorded during MVC. Normalized H-reflex (H max/M max) was significantly depressed pre-exercise in hypoxia compared with normoxia (0.31 ± 0.08 and 0.36 ± 0.08, respectively, P < 0.05). Hypoxia did not affect time to task failure (mean time of 453.9 ± 32.0 s) and MVC decrease at task failure (-18% in normoxia vs. -16% in hypoxia). At task failure, VA (-8%), RMSmax/M sup (-11%), H max/M max (-27%) and V sup/M sup (-37%) decreased (P < 0.05), but with no FiO2 effect. H max/M max restored significantly throughout recovery in hypoxia but not in normoxia, while V sup/M sup restored significantly during recovery in normoxia but not in hypoxia (P < 0.05). Collectively, these findings indicate that central adaptations resulting from sustained submaximal fatiguing contraction were not different in hypoxia and normoxia at task failure. However, the FiO₂-induced differences in spinal loop properties pre-exercise and throughout recovery suggest possible specific mediation by the hypoxic-sensitive group III and IV muscle afferents, supraspinal regulation mechanisms being mainly involved in hypoxia while spinal ones may be predominant in normoxia.

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Section: Introductionmentioning

confidence: 98%

Modulation of exercise-induced spinal loop properties in response to oxygen availability

et al. 2014

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“…This work was mainly carried out in cortical neurons at day 8 because the neurons are sensitive to hypoxic stress and DOR inhibition at this age as shown in our previous work (Hong et al, 2004;Zhang et al, 2000Zhang et al, ,2002. To compare neuronal responses to different stresses, we exposed cortical neurons to either hypoxia, naltrindole or both since MAP kinases are involved in DOR signaling and DOR inhibition can leads to neuronal injury (Zhang et al, 2002).…”

Section: Resultsmentioning

confidence: 99%

Anisomycin protects cortical neurons from prolonged hypoxia with differential regulation of p38 and ERK

et al. 2007

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MAP kinase is associated with delta-opioid receptor (DOR) signaling and plays a role in cell survival/ death. Since anisomycin may alter MAP kinase activity and affect neuronal survival, we investigated whether anisomycin alters neuronal response to hypoxic stress and DOR inhibition. The experiments were performed in cultured cortical neurons. MAP kinase activities were determined by immunoblotting and neuronal viability was assessed by LDH leakage and live/dead morphological study. DOR inhibition with naltrindole (10 μM) led to significant injury in normoxic neurons after 24 hours of treatment and exacerbated hypoxia-induced injury. Along with the injury, either by hypoxia or naltrindole, phosphorylated p38 increased in a major way, while phosphorylated ERK and JNK had no significant change or slightly decreased. Anisomycin (50 ng/ml) prevented the increase in phosphorylated p38 immunoreactivity induced by naltrindole and reduced the neuronal injury. The results suggest that 1) MAP kinases are differentially involved in neuronal response to hypoxia and DOR inhibition in cortical neurons with phosphorylated p38 immunoreactivity being up-regulated and 2) Anisomycin attenuates the increase in phosphorylated p38 immunoreactivity and reduces neuronal injury induced by hypoxia-and DOR inhibition.

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“…The capacity for central neurons to carry out anaerobic glycolysis in fact depends on several complex factors including the supply of glucose, mitochondrial function, and the activity or expression of glycolytic enzymes. 46 An increase in glycolytic capacity secondary to upregulation of these enzymes has been described in astrocytes subjected to hypoxia. 47 Glutamate A statistically nonsignificant (P = 0.052) positive correlation was found between glutamate levels and the ischemic score (r = 0.107).…”

Section: Pyruvatementioning

confidence: 99%

Quantitation of Ischemic Events After Severe Traumatic Brain Injury in Humans: A Simple Scoring System

Mazzeo

Kunene

Choi

et al. 2006

Journal of Neurosurgical Anesthesiology

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Effect of protein kinases on lactate dehydrogenase activity in cortical neurons during hypoxia

Cited by 26 publications

References 24 publications

Modulation of exercise-induced spinal loop properties in response to oxygen availability

Modulation of exercise-induced spinal loop properties in response to oxygen availability

Anisomycin protects cortical neurons from prolonged hypoxia with differential regulation of p38 and ERK

Quantitation of Ischemic Events After Severe Traumatic Brain Injury in Humans: A Simple Scoring System

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