scholarly journals Environmental Enrichment Enhances Cav 2.1 Channel-Mediated Presynaptic Plasticity in Hypoxic–Ischemic Encephalopathy

2021 ◽  
Vol 22 (7) ◽  
pp. 3414
Author(s):  
Suk-Young Song ◽  
Soonil Pyo ◽  
Sungchul Choi ◽  
Hee Sang Oh ◽  
Jung Hwa Seo ◽  
...  
Keyword(s):  
Environmental Enrichment ◽  
Hypoxic Condition ◽  
Hypoxic Ischemic Encephalopathy ◽  
Neuroprotective Effects ◽  
Y Maze ◽  
Behavioral Assessments ◽  
The Right ◽  
Vesicle Cycle ◽  
Ischemic Encephalopathy ◽  
Presynaptic Proteins

Hypoxic–ischemic encephalopathy (HIE) is a devastating neonatal brain condition caused by lack of oxygen and limited blood flow. Environmental enrichment (EE) is a classic paradigm with a complex stimulation of physical, cognitive, and social components. EE can exert neuroplasticity and neuroprotective effects in immature brains. However, the exact mechanism of EE on the chronic condition of HIE remains unclear. HIE was induced by a permanent ligation of the right carotid artery, followed by an 8% O2 hypoxic condition for 1 h. At 6 weeks of age, HIE mice were randomly assigned to either standard cages or EE cages. In the behavioral assessments, EE mice showed significantly improved motor performances in rotarod tests, ladder walking tests, and hanging wire tests, compared with HIE control mice. EE mice also significantly enhanced cognitive performances in Y-maze tests. Particularly, EE mice showed a significant increase in Cav 2.1 (P/Q type) and presynaptic proteins by molecular assessments, and a significant increase of Cav 2.1 in histological assessments of the cerebral cortex and hippocampus. These results indicate that EE can upregulate the expression of the Cav 2.1 channel and presynaptic proteins related to the synaptic vesicle cycle and neurotransmitter release, which may be responsible for motor and cognitive improvements in HIE.

Neuroprotective effects of hypothermia in inflammatory‐sensitized hypoxic‐ischemic encephalopathy

2016 ◽  
Vol 55 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Mathilde Chevin ◽  
Clémence Guiraut ◽  
Caroline Maurice‐Gelinas ◽  
Jessica Deslauriers ◽  
Sylvain Grignon ◽  
...  
Keyword(s):  
Hypoxic Ischemic Encephalopathy ◽  
Neuroprotective Effects ◽  
Ischemic Encephalopathy

scholarly journals Efficacy of different treatment times of mild cerebral hypothermia on oxidative factors and neuroprotective effects in neonatal patients with moderate/severe hypoxic–ischemic encephalopathy

2020 ◽  
Vol 48 (9) ◽  
pp. 030006052094377
Author(s):  
Tingting Yang ◽  
Shan Li
Keyword(s):  
Mild Hypothermia ◽  
Neuron Specific Enolase ◽  
The Other ◽  
Hypoxic Ischemic Encephalopathy ◽  
Psychomotor Development ◽  
Controlled Study ◽  
Neurological Assessment ◽  
Neuroprotective Effects ◽  
Assessment Scores ◽  
Ischemic Encephalopathy

Objective To investigate the efficacy of different treatment times of mild cerebral hypothermia for treating moderate/severe hypoxic–ischemic encephalopathy (HIE) in neonatal patients and its effects on oxidative factors. Methods This prospective, randomized, controlled study included 92 neonatal patients with moderate/severe HIE and 30 controls. The patients with HIE received routine treatment, 48 hours of hypothermia, or 72 hours of hypothermia. Results Superoxide dismutase (SOD) values were significantly lower and malondialdehyde (MDA) and neuron-specific enolase (NSE) values were higher in patients with HIE than in controls before the study. After 24, 48, and 72 hours of treatment, SOD values in all patients with HIE gradually increased and MDA and NSE values gradually decreased. At 3, 7, and 10 days, the Neonatal Behavioral Neurological Assessment scores were highest in the mild hypothermia for 72 hours group than in the other groups. The Mental and Psychomotor Development Indices scores of the Bayley Scales were significantly higher in the mild hypothermia for 72 hours group than in the other groups. Conclusion Hypothermia treatment of 72 hours is better than 48 hours for improving oxidative conditions, reducing NSE values, and improving neurological behavior and development for neonates with moderate/severe HIE.

scholarly journals The role of G-CSF neuroprotective effects in neonatal hypoxic-ischemic encephalopathy (HIE): current status

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
John Sieh Dumbuya ◽  
Lu Chen ◽  
Jang-Yen Wu ◽  
Bin Wang
Keyword(s):  
Ex Vivo ◽  
Neuroprotective Effect ◽  
Hypoxic Ischemic Encephalopathy ◽  
Cell Swelling ◽  
Current Status ◽  
Clinical Practices ◽  
Neonatal Brain ◽  
Neuroprotective Effects ◽  
Ischemic Encephalopathy ◽  
Stimulation Of

AbstractHypoxic-ischemic encephalopathy (HIE) is an important cause of permanent damage to central nervous system (CNS) that may result in neonatal death or manifest later as mental retardation, epilepsy, cerebral palsy, or developmental delay. The primary cause of this condition is systemic hypoxemia and/or reduced cerebral blood flow with long-lasting neurological disabilities and neurodevelopmental impairment in neonates. About 20 to 25% of infants with HIE die in the neonatal period, and 25-30% of survivors are left with permanent neurodevelopmental abnormalities. The mechanisms of hypoxia-ischemia (HI) include activation and/or stimulation of myriad of cascades such as increased excitotoxicity, oxidative stress, N-methyl-d-aspartic acid (NMDA) receptor hyperexcitability, mitochondrial collapse, inflammation, cell swelling, impaired maturation, and loss of trophic support. Different therapeutic modalities have been implicated in managing neonatal HIE, though translation of most of these regimens into clinical practices is still limited. Therapeutic hypothermia, for instance, is the most widely used standard treatment in neonates with HIE as studies have shown that it can inhibit many steps in the excito-oxidative cascade including secondary energy failure, increases in brain lactic acid, glutamate, and nitric oxide concentration. Granulocyte-colony stimulating factor (G-CSF) is a glycoprotein that has been implicated in stimulation of cell survival, proliferation, and function of neutrophil precursors and mature neutrophils. Extensive studies both in vivo and ex vivo have shown the neuroprotective effect of G-CSF in neurodegenerative diseases and neonatal brain damage via inhibition of apoptosis and inflammation. Yet, there are still few experimentation models of neonatal HIE and G-CSF’s effectiveness, and extrapolation of adult stroke models is challenging because of the evolving brain. Here, we review current studies and/or researches of G-CSF’s crucial role in regulating these cytokines and apoptotic mediators triggered following neonatal brain injury, as well as driving neurogenesis and angiogenesis post-HI insults.

scholarly journals Neuroprotective effects of electroacupuncture on hypoxic-ischemic encephalopathy in newborn rats association with increased expression of mTOR

2016 ◽  
Vol 11 ◽  
pp. S98-S105
Author(s):  
Tao Xu ◽  
Na Zhao ◽  
Jing-Dong Liu ◽  
Mo Xiao-Mei ◽  
Hui Zhang ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Molecular Mechanisms ◽  
Neuronal Damage ◽  
Statistical Significance ◽  
Mrna Level ◽  
Hypoxic Ischemic Encephalopathy ◽  
Therapeutic Effects ◽  
Model Group ◽  
Neuroprotective Effects ◽  
Ischemic Encephalopathy

In this study, we observed the therapeutic effects of acupuncture and investigated the underlying molecular mechanisms by constructed a hypoxic-ischemic encephalopathy (HIE) animal model. In the electroacupuncture group, mTOR expression increased since 1d, and continued to rise till the 21st day. All of the differences were significantly (p<0.05 vs the model group). Meanwhile, mTOR expression was analyzed by Western blotting. There was statistical significance between the model group and the electroacupuncture group in the four time periods (p<0.05). The results provide evidence that electroacupuncture treatment protected cortical neurons against HIE-induced neuronal damage and degenerative changes in rats, which is in association with activation of mTOR both at the mRNA level and protein level. Therefore, electroacupuncture may become a potential therapeutic strategy for HIE of newborn. 

Neuroprotective Agents for Neonates with Hypoxic-Ischemic Encephalopathy

2021 ◽  
Vol 40 (6) ◽  
pp. 406-413
Author(s):  
Keliana O'Mara ◽  
Christopher McPherson
Keyword(s):  
Therapeutic Hypothermia ◽  
Ischemic Injury ◽  
Hypoxic Ischemic Encephalopathy ◽  
Neuroprotective Agents ◽  
Neuroprotective Effects ◽  
Animal Data ◽  
Neurodevelopmental Impairment ◽  
Pharmacologic Agents ◽  
Ischemic Encephalopathy

Hypoxic-ischemic encephalopathy (HIE) remains a significant source of long-term neurodevelopmental impairment despite overall improvements in survival without disability in neonates who undergo therapeutic hypothermia. Each phase in the evolution of hypoxic-ischemic injury presents potential pharmacologic targets for neuroprotective agents. Melatonin is a promising emerging therapy for early phases of ischemic injury, but utility is currently limited by the lack of pharmaceutical-grade products. Magnesium has been extensively studied for its neuroprotective effects in the preterm population. Studies in neonates with HIE have produced mixed outcomes. Erythropoietin use in HIE with or without therapeutic hypothermia appears to be safe and may provide additional benefit. Dexmedetomidine, N-acetylcysteine, xenon, and topiramate all have promising animal data, but need additional human trials to elucidate what role they may play in HIE. Frequent review of existing literature is required to ensure provision of evidence-based pharmacologic agents for neuroprotection following HIE.

Sign in / Sign up

Export Citation Format

Share Document