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Candelario‐Jalil, Eduardo; Mhadu, Noël H.; González-Falcón, Armando; García-Cabrera, Michel; Muñóz, Eduardo; León, Olga Sonia; Fiebich, Bernd L.

doi:10.1186/1742-2094-2-3

Cited by 49 publications

(12 citation statements)

References 52 publications

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“…Transgenic rats and non-Tg littermates were tested serially for motor function before and for 28 days after focal cerebral ischemia using a Rotarod (Economex; Columbus Instruments, Columbus, OH), with slight modfications described by Candelario-Jalil and colleagues [ 45 ]. The rotating rod was fitted with dividers to accommodate rats.…”

Section: Methodsmentioning

confidence: 99%

The TNFα-Transgenic Rat: Hippocampal Synaptic Integrity, Cognition, Function, and Post-Ischemic Cell Loss

Pettigrew

Norris

2016

PLoS ONE

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The cytokine, tumor necrosis factor α (TNFα), is a key regulator of neuroinflammation linked to numerous neurodegenerative conditions and diseases. The present study used transgenic rats that overexpress a murine TNFα gene, under the control of its own promoter, to investigate the impact of chronically elevated TNFα on hippocampal synaptic function. Neuronal viability and cognitive recovery in TNFα Tg rats were also determined following an ischemic insult arising from reversible middle cerebral artery occlusion (MCAO). Basal CA3-CA1 synaptic strength, recorded in acute brain slices, was not significantly different between eight-week-old TNFα Tg rats and non-Tg rats. In contrast, slices from TNFα Tg rats showed significantly greater levels of long-term potentiation (LTP) in response to 100 Hz stimulation, suggesting that synaptic networks may be hyperexcitable in the context of elevated TNFα. Cognitive and motor deficits (assessed on the Morris Water Maze and Rotarod task, respectively) were present in TNFα Tg rats in the absence of significant differences in the loss of cortical and hippocampal neurons. TNF overexpression exacerbated MCAO-dependent deficits on the rotarod, but ameliorated cortical neuron loss in response to MCAO.

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Section: Methodsmentioning

confidence: 99%

The TNFα-Transgenic Rat: Hippocampal Synaptic Integrity, Cognition, Function, and Post-Ischemic Cell Loss

Pettigrew

Norris

2016

PLoS ONE

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“…The general neurological function of rats after MCAO was evaluated according to a six‐point neurological score system immediately before their euthanasia for brain collection 21. The criteria are: 0: no observable neurological deficits; 1: failure to fully extend the left forepaw; 2: circling to the left while moving in the cage; 3: falling to the left side; 4: no spontaneous walking with a depressed level of consciousness; 5: death.…”

Section: Methodsmentioning

confidence: 99%

“…Supplemental doses of equithesin were given as needed. Surgical procedures for MCAO follow that of Candelario-Jalil et al 18 Briefly, the right common carotid artery (CCA), the external carotid artery (ECA), and the internal carotid artery (ICA) were surgically exposed through a midline cervical incision. The arteries were separated from the adjacent vagus nerve and the surrounding connective tissue.…”

Section: Surgerymentioning

confidence: 99%

Direct profiling of phospholipids and lysophospholipids in rat brain sections after ischemic stroke

Wang

Liu

et al. 2010

Rapid Comm Mass Spectrometry

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Stroke, a deleterious cerebrovascular event, is caused by a critical reduction in the blood flow to the brain parenchyma that leads to brain injury and loss of brain functions. The inflammatory responses following ischemia often aggravate the neurological damage. Several pro-inflammatory mediators released after stroke are closely related to the metabolism of phospholipids. In this study we directly profiled the changes in phospholipids in the infarcted rat cerebral cortex 24 hours after middle cerebral artery occlusion (MCAO) using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). Several phosphatidylcholine (PC) species and sphingomyelin (SM) were significantly decreased after infarction. The cationization pattern of the remaining PCs showed a prominent shift from a mostly potassiated or protonated form to a predominantly sodiated pattern. Stroke also elevated the lysophosphatidylcholines (LPCs) and heme in tissue. The isobaric pairs in PC and LPC classes were resolved by masses through their respective alkali metal adducts in the presence of CsCl. The major fatty acyl LPC species were also structurally confirmed by MALDI-MS/MS. Overall, the results described the changes in PC and LPC species in the infarcted rat cortex. The elevated tissue levels of LPCs and heme signify the ongoing pathological lipid breakdown and the state of parenchymal inflammation. The elevated LPC level in tissue suggests a means of intervention through lysophospholipid metabolism that could potentially benefit the management of stroke and other acute neurological injuries.

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“…Similar to ibuprofen, acute treatment with nimesulide has been shown to reduce infarction volume and decrease neurological deficits in dose-dependent manner (Candelario-Jalil et al, 2004), and the neuroprotective effect was associated with decreased levels of prostaglandin E2 in the stroke brain. In another study, it was found that nimesulide reduced infarction volume and promoted behavioral recovery when the first dose was given within 2 hours after permanent MCAo in rats (Candelario-Jalil et al, 2005). Moreover, in a study where meloxicam was given 1 hour before surgery and then again after 24 hours it was found that it reduced infarction volume in permanent MCAo model in mice (Jacobsen et al, 2013).…”

Section: Other Pharmacological Modulations Of Inflammatory Signalimentioning

confidence: 99%

Role of microglia in ischemic focal stroke and recovery: focus on Toll-like receptors

Anttila

Whitaker

Wires

et al. 2017

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Stroke is the leading cause of disability in adults. Drug treatments that target stroke-induced pathological mechanisms and promote recovery are desperately needed. In the brain, an ischemic event triggers major inflammatory responses that are mediated by the resident microglial cells. In this review, we focus on the microglia activation after ischemic brain injury as a target of immunomodulatory therapeutics. We divide the microglia-mediated events following ischemic stroke into three categories: acute, subacute, and long-term events. This division encompasses the spatial and temporal dynamics of microglia as they participate in the pathophysiological changes that contribute to the symptoms and sequela of a stroke. The importance of Toll-like receptor (TLR) signaling in the outcomes of these pathophysiological changes is highlighted. Increasing evidence shows that microglia have a complex role in stroke pathophysiology and they mediate both detrimental and beneficial effects on stroke outcome. So far, most of the pharmacological studies in experimental models of stroke have focused on neuroprotective strategies which are impractical for clinical applications. Post-ischemic inflammation is long lasting and thus, could provide a therapeutic target for novel delayed drug treatment. However, more studies are needed to elucidate the role of microglia in the recovery process from an ischemic stroke and to evaluate the therapeutic potential of modulating post-ischemic inflammation to promote functional recovery.

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Cited by 49 publications

References 52 publications

The TNFα-Transgenic Rat: Hippocampal Synaptic Integrity, Cognition, Function, and Post-Ischemic Cell Loss

The TNFα-Transgenic Rat: Hippocampal Synaptic Integrity, Cognition, Function, and Post-Ischemic Cell Loss

Direct profiling of phospholipids and lysophospholipids in rat brain sections after ischemic stroke

Role of microglia in ischemic focal stroke and recovery: focus on Toll-like receptors

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