Fluoro-Jade B: a high affinity fluorescent marker for the localization of neuronal degeneration

Schmued, Larry C.; Hopkins, Keri J

doi:10.1016/s0006-8993(00)02513-0

Cited by 1,171 publications

(887 citation statements)

References 6 publications

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“…After embedded in Tissue‐Tek OCT, brains were sectioned at 20 μ m thickness. Fluoro‐Jade B staining was conducted as described previously 22. Tissues were first placed in 0.1 mol/L phosphate buffer.…”

Section: Methodsmentioning

confidence: 99%

Rapamycin prevents cerebral stroke by modulating apoptosis and autophagy in penumbra in rats

Zhang

Kai

et al. 2017

Ann Clin Transl Neurol

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ObjectiveWhether activation or inhibition of the mTOR pathway is beneficial to ischemic injury remains controversial. It may result from the different reaction of ischemic penumbra and core to modulation of mTOR pathway after cerebral ischemia–reperfusion injury in rats.MethodsLonga's middle cerebral artery occlusion (MCAO) method was conducted to induce the focal cerebral ischemia–reperfusion. Western blot analysis was used to examine the protein expression involving mTOR pathway, apoptosis, and autophagy‐related proteins. TTC staining and Fluoro‐Jade B staining was conducted to detect the infarct volume and cell apoptosis, respectively. Neurological function was measured by modified neurological severity score and left‐biased swing.Results mTOR signaling pathway was activated in ischemic penumbra and decreased in ischemic core after ischemia and ischemia–reperfusion. Ischemia–reperfusion injury induced the increase in cleaved caspase 9 and caspase 3 both in ischemic penumbra and in ischemic core, whereas the expression of phosphorylated ULK1, Beclin 1 and LC3‐II was decreased. Rapamycin pre or postadministration inhibited the overactivation of mTOR pathway in ischemic penumbra. Ameliorated neurological function and reduced infarct volume were observed after pre or postrapamycin treatment. Rapamycin markedly decreased the number of FJB‐positive cells and the expression of cleaved caspase‐3 and cleaved caspase‐9 proteins as well as increased the activation of autophagy reflected by ULK1, Beclin‐1 and LC3.Interpretation mTOR signaling pathway was activated in ischemic penumbra after cerebral ischemia–reperfusion injury in rats. mTOR inhibitor rapamycin significantly decreased the mTOR activation and infarct volume and subsequently improved neurological function. These results may relate to inhibition of neuron apoptosis and activation of autophagy.

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Section: Methodsmentioning

confidence: 99%

Rapamycin prevents cerebral stroke by modulating apoptosis and autophagy in penumbra in rats

Zhang

Kai

et al. 2017

Ann Clin Transl Neurol

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“…Cryostat sections (25 mm) were mounted on superfrostedcoated slides (Fisher Scientific, Pittsburgh, PA, USA). Fluoro-Jade B staining was performed as described by Schmued and Hopkins (2000) (Suh et al, 2003). In brief, the slides were immersed in a basic alcohol solution followed by 0.06% potassium permanganate.…”

Section: Histological Evaluations Of Neuronal Deathmentioning

confidence: 99%

Prevention of Acute/Severe Hypoglycemia-Induced Neuron Death by Lactate Administration

Won

Jang

Yoo

et al. 2012

J Cereb Blood Flow Metab

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Hypoglycemia-induced cerebral neuropathy can occur in patients with diabetes who attempt tight control of blood glucose and may lead to cognitive dysfunction. Accumulating evidence from animal models suggests that hypoglycemia-induced neuronal death is not a simple result of glucose deprivation, but is instead the end result of a multifactorial process. In particular, the excessive activation of poly (ADP-ribose) polymerase-1 (PARP-1) consumes cytosolic nicotinamide adenine dinucleotide (NAD + ), resulting in energy failure. In this study, we investigate whether lactate administration in the absence of cytosolic NAD + affords neuroprotection against hypoglycemiainduced neuronal death. Intraperitoneal injection of sodium L-lactate corrected arterial blood pH and blood lactate concentration after hypoglycemia. Lactate administered without glucose was not sufficient to promote electroencephalogram recovery from an isoelectric state during hypoglycemia. However, supplementation of glucose with lactate reduced neuronal death by B80% in the hippocampus. Hypoglycemia-induced superoxide production and microglia activation was also substantially reduced by administration of lactate. Taken together, these results suggest an intriguing possibility: that increasing brain lactate following hypoglycemia offsets the decrease in NAD + due to overactivation of PARP-1 by acting as an alternative energy substrate that can effectively bypass glycolysis and be fed directly to the citric acid cycle to maintain cellular ATP levels.

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“…The sections were stained with Fluoro-Jade B to identify degenerating neurons, as previously described. 35 FluoroJade B staining signals were detected at an excitation of 480 nm and an emission of 525 nm under an epifluorescence microscope with a Â 5 objective, and captured with a SPOT-RT 3-chip digital camera (Diagnostic Instruments Inc., Sterling Heights, MI, USA). The infarct volume was calculated using an image processing and analysis system (Q570IW; Leica).…”

Section: Fluoro-jade B Staining and Measurement Of Infarct Volumementioning

confidence: 99%

Excision repair cross-complementing 1 expression protects against ischemic injury following middle cerebral artery occlusion in the rat brain

Yang

Shen

et al. 2009

Gene Ther

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To study the effects of excision repair cross-complementing 1 (ERCC1) on the pathophysiological process of brain ischemia, we examined the changes in ERCC1 expression, as well as the functional significance of ERCC1 in the rat brain following middle cerebral artery occlusion (MCAO). The results were as follows: (1) ERCC1 immunopositive cells were widely distributed in various brain regions. ERCC1 expression was localized to the nuclei of neurons and astrocytes. (2) ERCC1 expression, as determined by western blot, increased at 3 days, remaining until 14 days, in the ipsilateral cortex and striatum following MCAO. Immunohistochemical analysis demonstrated that ischemia induced increased ERCC1 expression within the periinfarct core, with increasingly less expression toward the core. (3) Knockdown of ERCC1 expression by intraventricular injection of antisense plasmids increased DNA damage and infarct volume in the ischemic brain. (4) ERCC1 overproduction, by injection of expression plasmids, significantly reduced infarct volume and the accumulation of DNA-damaged neurons. Taken together, these results indicate that both endogenous ERCC1 and exogenous ERCC1 have an important neuroprotective function in the brain. In addition, administration of ERCC1 to the brain could prove to be a successful strategy for neuronal protection against ischemic injury.

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Fluoro-Jade B: a high affinity fluorescent marker for the localization of neuronal degeneration

Cited by 1,171 publications

References 6 publications

Rapamycin prevents cerebral stroke by modulating apoptosis and autophagy in penumbra in rats

Rapamycin prevents cerebral stroke by modulating apoptosis and autophagy in penumbra in rats

Prevention of Acute/Severe Hypoglycemia-Induced Neuron Death by Lactate Administration

Excision repair cross-complementing 1 expression protects against ischemic injury following middle cerebral artery occlusion in the rat brain

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