Differential spread of anoxic depolarization contributes to the pattern of neuronal injury after oxygen and glucose deprivation (OGD) in the Substantia Nigra in rat brain slices

Neuroscience ◽  
2017 ◽  
Vol 340 ◽  
pp. 359-372 ◽  
Author(s):  
Rashika N. Karunasinghe ◽  
Angus C. Grey ◽  
Ravindra Telang ◽  
Srdjan M. Vlajkovic ◽  
Janusz Lipski
Keyword(s):  
Substantia Nigra ◽  
Rat Brain ◽  
Brain Slices ◽  
Neuronal Injury ◽  
Glucose Deprivation ◽  
Oxygen And Glucose Deprivation ◽  
Anoxic Depolarization

Neuroprotective Effects of Cactus Polysaccharide on Oxygen and Glucose Deprivation Induced Damage in Rat Brain Slices

2007 ◽  
Vol 28 (4) ◽  
pp. 559-568 ◽  
Author(s):  
Xianju Huang ◽  
Qin Li ◽  
Yingpei Zhang ◽  
Qing Lü ◽  
Lianjun Guo ◽  
...  
Keyword(s):  
Rat Brain ◽  
Brain Slices ◽  
Glucose Deprivation ◽  
Neuroprotective Effects ◽  
Oxygen And Glucose Deprivation

scholarly journals Neuroprotective Effects of Intranasal IGF-1 against Neonatal Lipopolysaccharide-Induced Neurobehavioral Deficits and Neuronal Inflammation in the Substantia Nigra and Locus Coeruleus of Juvenile Rats

2017 ◽  
Vol 39 (6) ◽  
pp. 443-459 ◽  
Author(s):  
Lu-Tai Tien ◽  
Yih-Jing Lee ◽  
Yi Pang ◽  
Silu Lu ◽  
Jonathan W. Lee ◽  
...  
Keyword(s):  
Substantia Nigra ◽  
Locus Coeruleus ◽  
Rat Brain ◽  
Neuronal Injury ◽  
Cyclooxygenase 2 ◽  
Brain Inflammation ◽  
Intracerebral Injection ◽  
Behavioral Disturbances ◽  
Th Cells ◽  
Juvenile Rats

Neonatal lipopolysaccharide (LPS) exposure-induced brain inflammation resulted in motor dysfunction and brain dopaminergic neuronal injury, and increased the risks of neurodegenerative disorders in adult rats. Our previous studies showed that intranasal administration of insulin-like growth factor-1 (IGF-1) protects against LPS-induced white matter injury in the developing rat brain. To further examine whether IGF-1 protects against LPS-induced brain neuronal injury and neurobehavioral dysfunction, recombinant human IGF-1 (rhIGF-1) at a dose of 50 µg/pup was administered intranasally 1 h following intracerebral injection of LPS (1 mg/kg) in postnatal day 5 (P5) Sprague-Dawley rat pups. Neurobehavioral tests were carried out from P7 to P21, and brain neuronal injury was examined at P21. Our results showed that LPS exposure resulted in disturbances of motor behaviors in juvenile rats. Moreover, LPS exposure caused injury to central catecholaminergic neurons, as indicated by a reduction of tyrosine hydroxylase (TH) immunoreactivity in the substantia nigra (SN), ventral tegmental area (VTA) and olfactory bulb (OB), and brain noradrenergic neurons, as indicated by a reduction of TH immunoreactivity in the locus coeruleus (LC) of the P21 rat brain. The LPS-induced reduction of TH+ cells was observed at a greater degree in the SN and LC of the P21 rat brain. Intranasal rhIGF-1 treatment attenuated LPS-induced central catecholaminergic neuronal injury and motor behavioral disturbances, including locomotion, beam walking test and gait analysis. Intranasal rhIGF-1 administration also attenuated LPS-induced elevation of IL-1β levels and numbers of activated microglia, and cyclooxygenase-2+ cells, which were double labeled with TH+ cells in the SN, VTA, OB and LC of the P21 rat brain. These results suggest that IGF-1 may provide protection against neonatal LPS exposure-induced central catecholaminergic neuronal injury and motor behavioral disturbances, and that the protective effects are associated with the inhibition of microglia activation and the reduction of neuronal oxidative stress by the suppression of the neuronal cyclooxygenase-2 expression.

Hyperhomocysteinemia increases damage on brain slices exposed to in vitro model of oxygen and glucose deprivation: prevention by folic acid

2006 ◽  
Vol 24 (4) ◽  
pp. 285-291 ◽  
Author(s):  
Bárbara Tagliari ◽  
Lauren L. Zamin ◽  
Christianne G. Salbego ◽  
Carlos Alexandre Netto ◽  
Angela T.S. Wyse
Keyword(s):  
Folic Acid ◽  
In Vitro Model ◽  
Brain Slices ◽  
Glucose Deprivation ◽  
Oxygen And Glucose Deprivation ◽  
Vitro Model

scholarly journals Protective Role of Kv7 Channels in Oxygen and Glucose Deprivation-Induced Damage in Rat Caudate Brain Slices

2015 ◽  
Vol 35 (10) ◽  
pp. 1593-1600 ◽  
Author(s):  
Vincenzo Barrese ◽  
Maurizio Taglialatela ◽  
Iain A Greenwood ◽  
Colin Davidson
Keyword(s):  
Cell Death ◽  
Brain Slices ◽  
Peak Level ◽  
Glucose Deprivation ◽  
Wistar Rat ◽  
Protective Role ◽  
Triphenyltetrazolium Chloride ◽  
Lactate Dehydrogenase Activity ◽  
Oxygen And Glucose Deprivation ◽  
Dopamine Efflux

Ischemic stroke can cause striatal dopamine efflux that contributes to cell death. Since Kv7 potassium channels regulate dopamine release, we investigated the effects of their pharmacological modulation on dopamine efflux, measured by fast cyclic voltammetry (FCV), and neurotoxicity, in Wistar rat caudate brain slices undergoing oxygen and glucose deprivation (OGD). The Kv7 activators retigabine and ICA27243 delayed the onset, and decreased the peak level of dopamine efflux induced by OGD; and also decreased OGD-induced damage measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining. Retigabine also reduced OGD-induced necrotic cell death evaluated by lactate dehydrogenase activity assay. The Kv7 blocker linopirdine increased OGD-evoked dopamine efflux and OGD-induced damage, and attenuated the effects of retigabine. Quantitative-PCR experiments showed that OGD caused an ~ 6-fold decrease in Kv7.2 transcript, while levels of mRNAs encoding for other Kv7 subunits were unaffected; western blot experiments showed a parallel reduction in Kv7.2 protein levels. Retigabine also decreased the peak level of dopamine efflux induced by L-glutamate, and attenuated the loss of TTC staining induced by the excitotoxin. These results suggest a role for Kv7.2 in modulating ischemia-evoked caudate damage.

scholarly journals Somatic autophagy of axonal mitochondria in ischemic neurons

2019 ◽  
Vol 218 (6) ◽  
pp. 1891-1907 ◽  
Author(s):  
Yanrong Zheng ◽  
Xiangnan Zhang ◽  
Xiaoli Wu ◽  
Lei Jiang ◽  
Anil Ahsan ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Neuronal Injury ◽  
Glucose Deprivation ◽  
Retrograde Transport ◽  
Direct Link ◽  
Mitochondrial Content ◽  
Oxygen And Glucose Deprivation ◽  
Mitochondrial Movement ◽  
Mitochondrial Motility ◽  
Ischemic Neuronal Injury

Mitophagy protects against ischemic neuronal injury by eliminating damaged mitochondria, but it is unclear how mitochondria in distal axons are cleared. We find that oxygen and glucose deprivation-reperfusion reduces mitochondrial content in both cell bodies and axons. Axonal mitochondria elimination was not abolished in Atg7fl/fl;nes-Cre neurons, suggesting the absence of direct mitophagy in axons. Instead, axonal mitochondria were enwrapped by autophagosomes in soma and axon-derived mitochondria prioritized for elimination by autophagy. Intriguingly, axonal mitochondria showed prompt loss of anterograde motility but increased retrograde movement upon reperfusion. Anchoring of axonal mitochondria by syntaphilin blocked neuronal mitophagy and aggravated injury. Conversely, induced binding of mitochondria to dynein reinforced retrograde transport and enhanced mitophagy to prevent mitochondrial dysfunction and attenuate neuronal injury. Therefore, we reveal somatic autophagy of axonal mitochondria in ischemic neurons and establish a direct link of retrograde mitochondrial movement with mitophagy. Our findings may provide a new concept for reducing ischemic neuronal injury by correcting mitochondrial motility.

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