Applicability of the grip strength and automated von Frey tactile sensitivity tests in the mouse photothrombotic model of stroke

Alamri, Faisal; Shoyaib, Abdullah Al; Biggers, Abbie; Jayaraman, Srinidhi; Guindon, Josée; Karamyan, Vardan T.

doi:10.1016/j.bbr.2017.09.008

Cited by 49 publications

(24 citation statements)

References 51 publications

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“…Infarct volume was assessed with a direct method using ImageJ v2.1 (National Institutes of Health). The grip forces of the mice were measured as previously described ( 24 ).…”

Section: Methodsmentioning

confidence: 99%

NDRG2 attenuates ischemia-induced astrocyte necroptosis via the repression of RIPK1

et al. 2020

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Cerebral ischemia results in severe brain damage, and is a leading cause of death and long-term disability. Previous studies have investigated methods to activate astrocytes in order to promote repair in injured brain tissue and inhibit cell death. It has previously been shown that N-myc downstream-regulated gene 2 (NDRG2) was highly expressed in astrocytes and associated with cell activity, but the underlying mechanism is largely unknown. The present study generated NDRG2 conditional knockout ( Ndrg2 -/-) mice to investigate whether NDRG2 can block ischemia-induced astrocyte necroptosis by suppressing receptor interacting protein kinase 1 (RIPK1) expression. This study investigated astrocyte activity in cerebral ischemia, and identified that ischemic brain injuries could trigger RIP-dependent astrocyte necroptosis. The depletion of NDRG2 was found to accelerate permanent middle cerebral artery occlusion-induced necroptosis in the brain tissue of Ndrg2 -/- mice, indicating that NDRG2 may act as a neuroprotector during cerebral ischemic injury. The present study suggested that NDRG2 attenuated astrocytic cell death via the suppression of RIPK1. The pharmacological inhibition of astrocyte necroptosis by necrostatin-1 provided neuroprotection against ischemic brain injuries after NDRG2 knockdown. Therefore, NDRG2 could be considered as a potential target for the treatment of cerebral ischemia.

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“…Infarct volume was assessed with a direct method using ImageJ v2.1 (National Institutes of Health). The grip forces of the mice were measured as previously described ( 24 ).…”

Section: Methodsmentioning

confidence: 99%

NDRG2 attenuates ischemia-induced astrocyte necroptosis via the repression of RIPK1

et al. 2020

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“…This is a test to evaluate motor coordination function of rodents. This test was carried out according to the study by Alamri et al (Alamri et al, ). Mice walked on an elevated wire grid (12 mm square wire mesh with 33 cm/20 cm total area) for 2 min while being video‐recorded.…”

Section: Methodsmentioning

confidence: 99%

Prenatal electronic cigarette exposure decreases brain glucose utilization and worsens outcome in offspring hypoxic–ischemic brain injury

Sifat

Nozohouri

Villalba

et al. 2020

Journal of Neurochemistry

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It has been shown that prenatal nicotine and tobacco smoke exposure can cause different neurobehavioral disorders in the offspring. We hypothesize that prenatal exposure to nicotine‐containing electronic cigarette (e‐Cig) vapor can predispose newborn to enhanced sensitivity to hypoxic–ischemic (HI) brain injury and impaired motor and cognitive functions. In this study, pregnant CD1 mice were exposed to e‐Cig vapor (2.4% nicotine). Primary cortical neurons isolated from e‐Cig exposed fetus were exposed to oxygen–glucose deprivation followed by reoxygenation (OGD/R) to mimic HI brain injury. Cell viability and glucose utilization were analyzed in these neurons. HI brain injury was induced in 8–9‐day‐old pups. Short‐term brain injury was evaluated by triphenyltetrazolium chloride staining. Long‐term motor and cognitive functions were evaluated by open field, novel object recognition, Morris water maze, and foot fault tests. Western blotting and immunofluorescence were done to characterize glucose transporters in offspring brain. We found that e‐Cig exposed neurons demonstrated decreased cell viability and glucose utilization in OGD/R. Prenatally e‐Cig exposed pups also had increased brain injury and edema 24 hr after HI brain injury. Further, in utero e‐Cig exposed offspring with HI brain injury displayed impaired memory, learning, and motor coordination at adolescence. Additionally, the expression of glucose transporters decreased in e‐Cig exposed offspring brain after HI brain injury. These results indicate that reduced glucose utilization can contribute to prenatal e‐Cig exposure induced worsened HI brain injury in offspring. This study is instrumental in elucidating the possible deleterious effects of e‐Cig use in the general population.

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“…Grid‐walking test was carried out as previously described (Alamri et al ; Vijayan et al ). Mice walked on an elevated wire grid (12 mm square wire mesh with 33 cm/20 cm total area) for 5 min while being video‐recorded.…”

Section: Methodsmentioning

confidence: 99%

“…Cylinder test, mice were video‐recorded in a clear acrylic cylinder (17 cm height and 10 cm diameter) for 5 min to determine forelimb symmetry in exploratory rearing (Alamri et al ; Vijayan et al ). During each rear (usually closer to 20 are required for proper analysis) the use of the affected, unaffected, or both forelimbs was counted.…”

Section: Methodsmentioning

confidence: 99%

Peptidase neurolysin functions to preserve the brain after ischemic stroke in male mice

Jayaraman

Shoyaib

Kocot

et al. 2019

Journal of Neurochemistry

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Previous studies documented up‐regulation of peptidase neurolysin (Nln) after brain ischemia, however, the significance of Nln function in the post‐stroke brain remained unknown. The aim of this study was to assess the functional role of Nln in the brain after ischemic stroke. Administration of a specific Nln inhibitor Agaricoglyceride A (AgaA) to mice after stroke in a middle cerebral artery occlusion model, dose‐dependently aggravated injury measured by increased infarct and edema volumes, blood–brain barrier disruption, increased levels of interleukin 6 and monocyte chemoattractant protein‐1, neurological and motor deficit 24 h after stroke. In this setting, AgaA resulted in inhibition of Nln in the ischemic hemisphere leading to increased levels of Nln substrates bradykinin, neurotensin, and substance P. AgaA lacked effects on several physiological parameters and appeared non‐toxic to mice. In a reverse approach, we developed an adeno‐associated viral vector (AAV2/5‐CAG‐Nln) to overexpress Nln in the mouse brain. Applicability of AAV2/5‐CAG‐Nln to transduce catalytically active Nln was confirmed in primary neurons and in vivo. Over‐expression of Nln in the mouse brain was also accompanied by decreased levels of its substrates. Two weeks after in vivo transduction of Nln using the AAV vector, mice were subjected to middle cerebral artery occlusion and the same outcome measures were evaluated 72 h later. These experiments revealed that abundance of Nln in the brain protects animals from stroke. This study is the first to document functional significance of Nln in pathophysiology of stroke and provide evidence that Nln is an endogenous mechanism functioning to preserve the brain from ischemic injury.

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Applicability of the grip strength and automated von Frey tactile sensitivity tests in the mouse photothrombotic model of stroke

Cited by 49 publications

References 51 publications

NDRG2 attenuates ischemia-induced astrocyte necroptosis via the repression of RIPK1

NDRG2 attenuates ischemia-induced astrocyte necroptosis via the repression of RIPK1

Prenatal electronic cigarette exposure decreases brain glucose utilization and worsens outcome in offspring hypoxic–ischemic brain injury

Peptidase neurolysin functions to preserve the brain after ischemic stroke in male mice

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