Oxygen and glucose deprivation (OGD)-induced spreading depression in the Substantia Nigra

Karunasinghe, Rashika N.; Lipski, Janusz

doi:10.1016/j.brainres.2013.06.016

Cited by 23 publications

(15 citation statements)

References 73 publications

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“…Hypoxia and MPP + stress have been recognized as potential pathogenic factors that contribute to the development of PD [6,7]. Although the specific mechanism underlying neuron death in PD is not yet clearly understood, a large body of evidence strongly supports that mitochondrial dysfunction is evident in the brains of PD patients [30,31].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, as the morbidity of PD is greater among older people, it might be associated with age-related conditions such as prolonged ischemia or hypoxia in the brain. There is ample evidence to show that an insufficient blood or oxygen supply to the brain, could attenuate neurons’ resistance to environmental damage, and it can even trigger cell death [5,6,7]. Therefore, hypoxia/ischemia and neurotoxins should also be recognized as critical pathogenic factors that contribute to the development of PD.…”

Section: Introductionmentioning

confidence: 99%

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Cytoprotection against Hypoxic and/or MPP+ Injury: Effect of δ–Opioid Receptor Activation on Caspase 3

Zhi

Shao

et al. 2016

IJMS

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The pathological changes of Parkinson’s disease (PD) are, at least partially, associated with the dysregulation of PTEN-induced putative kinase 1 (PINK1) and caspase 3. Since hypoxic and neurotoxic insults are underlying causes of PD, and since δ-opioid receptor (DOR) is neuroprotective against hypoxic/ischemic insults, we sought to determine whether DOR activation could protect the cells from damage induced by hypoxia and/or MPP+ by regulating PINK1 and caspase 3 expressions. We exposed PC12 cells to either severe hypoxia (0.5%–1% O2) for 24–48 h or to MPP+ at different concentrations (0.5, 1, 2 mM) and then detected the levels of PINK1 and cleaved caspase 3. Both hypoxia and MPP+ reduced cell viability, progressively suppressed the expression of PINK1 and increased the cleaved caspase 3. DOR activation using UFP-512, effectively protected the cells from hypoxia and/or MPP+ induced injury, reversed the reduction in PINK1 protein and significantly attenuated the increase in the cleaved caspase 3. On the other hand, the application of DOR antagonist, naltrindole, greatly decreased cell viability and increased cleaved caspase 3. These findings suggest that DOR is cytoprotective against both hypoxia and MPP+ through the regulation of PINK1 and caspase 3 pathways.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cytoprotection against Hypoxic and/or MPP+ Injury: Effect of δ–Opioid Receptor Activation on Caspase 3

Zhi

Shao

et al. 2016

IJMS

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“…In fact, in RLS patients, as well as in those with migraine and aura, the SD model plays a role. This is particularly relevant as dopamine levels are reduced in several areas of the central nervous system, including the striatum and midbrain (dopaminergic cell group), which are two important regions for RLS circuitry [31,33]. Further investigations should therefore be conducted for RLS and SD.…”

Section: Discussionmentioning

confidence: 99%

Relationship between primary restless legs syndrome and migraine with aura

Acar

Alagöz

et al. 2016

The Kaohsiung J of Med Scie

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In this study, the prevalence and characteristics of definite migraine in primary restless legs syndrome (pRLS) patients and matched control patients (CPs) were investigated. We evaluated 63 consecutive adult pRLS patients and 141 age- and sex-matched controls in this case-control study. The diagnosis of migraine and its subtypes were defined based on The International Classification of Headache Disorders-II. Only those with "definite" migraine were included in the study. The mean age of 63 adult pRLS patients (15 men and 48 women) who participated in the study was 49.4 years. A total of 27 patients (42.9%) had definite migraine. Of these migraineurs, seven (11.1%) were without aura and 20 (31.8%) were with aura. The mean age of the 141 matched CPs was 48.7 years. A total of 32 CPs (22.7%) experienced migraine. Among these 32 migraineurs, 28 (19.9%) were without aura and four (2.8%) were with aura. Migraine and migraine with aura were significantly more common in pRLS patients than in CPs. pRLS patients with migraine were more anxious and experienced a shorter duration of RLS symptoms than pRLS patients without migraine. Migraineurs in the pRLS group tended to have high scores for severity of migraine headache by Visual Analog Scale score and high levels of disability by Migraine Disability Assessment grading than those in the control group. pRLS patients showed a positive association with definite migraine headaches. In contrast to results highlighted in recent studies, we found a strong link between migraine with aura and pRLS.

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“…As PD and some neurodegenerative diseases are mainly found in older populations , their pathogenesis might be associated with age‐related vasculopathy and related conditions that result in insufficient blood and/or oxygen supply to the brain . Indeed, hypoxic and/or ischemic stress has been recognized as one of pathogenic factors that contribute to the development of PD . Many people with ischemic/hypoxic brain injury (e.g., cerebral palsy in children, posthypoxic PD or dystonia in adults) develop movement disorders that can manifest weeks, months or even years after the predisposing event.…”

Section: Astrocytes and Pdmentioning

confidence: 99%

Deep Brain Stimulation: Are Astrocytes a Key Driver Behind the Scene?

Fenoy¹,

Goetz

Chabardès

et al. 2014

CNS Neurosci Ther

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Despite its widespread use, the underlying mechanism of deep brain stimulation (DBS) remains unknown. Once thought to impart a "functional inactivation", there is now increasing evidence showing that DBS actually can both inhibit neurons and activate axons, generating a wide range of effects. This implies that the mechanisms that underlie DBS work not only locally but also at the network level. Therefore, not only may DBS induce membrane or synaptic plastic changes in neurons over a wide network, but it may also trigger celllular and molecular changes in other cells, especially astrocytes, where together the glial-neuronal interactions may explain effects that are not clearly rationalized by simple activation/inhibition theories alone. Recent studies suggest that 1) High frequency stimulation (HFS) activates astrocytes and leads to the release of gliotransmitters that can regulate surrounding neurons at the synapse; 2) Activated astrocytes modulate synaptic activity and increase axonal activation; 3) Activated astrocytes can signal further astrocytes across large networks, contributing to observed network effects induced by DBS; 4) Activated astrocytes can help explain the disparate effects of activation and inhibition induced by HFS at different sites; 5) Astrocytes contribute to synaptic plasticity through long-term potentiation (LTP) and depression (LTD), possibly helping to mediate the long term effects of DBS; and 6) DBS may increase delta-opioid receptor activity in astrcoytes to confer neuroprotection. Together, the plastic changes in these glial-neuronal interactions network-wide likely underlie the range of effects seen, from the variable temporal latencies to observed effect to global activation patterns. This article reviews recent research progress in the literature on how astrocytes play a key role in DBS efficacy.

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Oxygen and glucose deprivation (OGD)-induced spreading depression in the Substantia Nigra

Cited by 23 publications

References 73 publications

Cytoprotection against Hypoxic and/or MPP+ Injury: Effect of δ–Opioid Receptor Activation on Caspase 3

Cytoprotection against Hypoxic and/or MPP+ Injury: Effect of δ–Opioid Receptor Activation on Caspase 3

Relationship between primary restless legs syndrome and migraine with aura

Deep Brain Stimulation: Are Astrocytes a Key Driver Behind the Scene?

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