Fluoro-Jade: Novel Fluorochromes for Detecting Toxicant-Induced Neuronal Degeneration

Schmued, Larry C.; Hopkins, Keri J

doi:10.1177/019262330002800111

Cited by 233 publications

(151 citation statements)

References 33 publications

(59 reference statements)

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“…Finally, the neurotoxic effects of MDMA may not be limited to serotonergic neurons. Schmued (2003) found that high doses of MDMA led to cellular damage in the rat forebrain (where no serotonergic somata are present) as indicated by staining with Fluoro-Jade B, a marker for neurodegeneration that has been validated with several known neurotoxins (Schmued and Hopkins, 2000).…”

Section: Discussionmentioning

confidence: 99%

Dissociation of the Neurochemical and Behavioral Toxicology of MDMA (‘Ecstasy’) by Citalopram

Piper

Fraiman

Owens

et al. 2007

Neuropsychopharmacol

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High or repeated doses of the recreational drug 3,4-methylenedioxymethamphetamine (MDMA, or 'Ecstasy') produce long-lasting deficits in several markers of serotonin (5-HT) system integrity and also alter behavioral function. However, it is not yet clear whether MDMA-induced serotonergic neurotoxicity is responsible for these behavioral changes or whether other mechanisms are involved. The present experiment tested the hypothesis that blocking serotonergic neurotoxicity by pretreatment with the selective 5-HT reuptake inhibitor citalopram will also prevent the behavioral and physiological consequences of an MDMA binge administration. Male, SpragueDawley rats (N ¼ 67) received MDMA (4 Â 10 mg/kg) with or without citalopram (10 mg/kg) pretreatment. Core temperature, ejaculatory response, and body weight were monitored during and immediately following drug treatments. A battery of tests assessing motor, cognitive, exploratory, anxiety, and social behaviors was completed during a 10-week period following MDMA administration. Brain tissue was collected at 1 and 10 weeks after drug treatments for measurement of regional 5-HT transporter binding and (for the 1-week samples) 5-HT and 5-HIAA concentrations. Citalopram pretreatment blocked MDMA-related reductions in aggressive and exploratory behavior measured in the social interaction and hole-board tests respectively. Such pretreatment also had the expected protective effect against MDMA-induced 5-HT neurotoxicity at 1 week following the binge. In contrast, citalopram did not prevent most of the acute effects of MDMA (eg hyperthermia and weight loss), nor did it block the decreased motor activity seen in the binge-treated animals 1 day after dosing. These results suggest that some of the behavioral and physiological consequences of a high-dose MDMA regimen in rats are mediated by mechanisms other than the drug's effects on the serotonergic system. Elucidation of these mechanisms requires further study of the influence of MDMA on other neurotransmitter systems.

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Section: Discussionmentioning

confidence: 99%

Dissociation of the Neurochemical and Behavioral Toxicology of MDMA (‘Ecstasy’) by Citalopram

Piper

Fraiman

Owens

et al. 2007

Neuropsychopharmacol

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“…One basic prerequisite is perfused tissue, otherwise erythrocytes will also be highlighted and interfere with signals from degenerating cells. Fluoro-Jade B is an anionic dye reportedly specific for soma and neurites of degenerating neurons under various pathologic conditions, including ischemia (Schmued and Hopkins, 2000), although there are reports that describe labeling of microglia and astrocytes under certain conditions (Damjanac et al, 2007;Saganova et al, 2006). Owing to the high sensitivity of Fluoro-Jade B, detection of degenerating neurons as early as 1.5 hours after a 90-minute MCAO in mice is possible (Liu et al, 2009).…”

Section: Light Microscopy and Macroscopymentioning

confidence: 99%

Visualizing Cell Death in Experimental Focal Cerebral Ischemia: Promises, Problems, and Perspectives

Zille

Farr

Przesdzing

et al. 2011

J Cereb Blood Flow Metab

125

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One of the hallmarks of stroke pathophysiology is the widespread death of many different types of brain cells. As our understanding of the complex disease that is stroke has grown, it is now generally accepted that various different mechanisms can result in cell damage and eventual death. A plethora of techniques is available to identify various pathological features of cell death in stroke; each has its own drawbacks and pitfalls, and most are unable to distinguish between different types of cell death, which partially explains the widespread misuse of many terms. The purpose of this review is to summarize the standard histopathological and immunohistochemical techniques used to identify various pathological features of stroke. We then discuss how these methods should be properly interpreted on the basis of what they are showing, as well as advantages and disadvantages that require consideration. As there is much interest in the visualization of stroke using noninvasive imaging strategies, we also specifically discuss how these techniques can be interpreted within the context of cell death.

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“…FJB staining was performed according to the method described by Schmued and Hopkins [28]. Additional sections were used to assess double-label fluorescence immunohistochemistry with FJB using primary antibody to glial fibrillary acidic protein (GFAP) or Neuronal Nuclei (NeuN) in a concentration of 1:1000 (GFAP) or 1:400 (NeuN), and a secondary antibody tagged with a fluorophore (Alexa Fluor 555, Invitrogen, Eugene, OR) in a concentration of 1:500.…”

Section: Fjb Histochemistrymentioning

confidence: 99%

“…Additional sections were used to assess double-label fluorescence immunohistochemistry with FJB using primary antibody to glial fibrillary acidic protein (GFAP) or Neuronal Nuclei (NeuN) in a concentration of 1:1000 (GFAP) or 1:400 (NeuN), and a secondary antibody tagged with a fluorophore (Alexa Fluor 555, Invitrogen, Eugene, OR) in a concentration of 1:500. FJB and 4'6'-diamidino-2-phenyllindole (DAPI) double staining was performed using previously described methods [28,35,41].…”

Section: Fjb Histochemistrymentioning

confidence: 99%

“…We hypothesized that the postnatal age alters the susceptibility to neuronal injury during acute hypoglycemia. FJB is a putative marker of degenerating neurons [28] and has been used to determine post-hypoglycemic cell injury in developing and mature rodent brains [32,35,41,42,44]. Rats of these ages were chosen due to the neurodevelopmental similarities with the pediatric populations at risk for hypoglycemia, namely, the preterm infant (P7), full term infant (P14) and young child (P28) [12].…”

Section: Introductionmentioning

confidence: 99%

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Postnatal age influences hypoglycemia-induced neuronal injury in the rat brain

et al. 2008

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Acute hypoglycemia is associated with neuronal injury in the mature human and rodent brains. Even though hypoglycemia is a common metabolic problem during development, its effects on the developing brain are not well understood. To characterize the severity of regional brain injury, postnatal day (P) 7, P14, P28 (N=20-30/age) and adult rats (N=8-12) were subjected to acute hypoglycemia of equivalent severity and duration (mean blood glucose concentration: 30.0±0.1 mg/ dL for 210 min). Neuronal injury in the cerebral cortex, striatum, hippocampus and hypothalamus was assessed 24 hr, 72 hr and 1 wk later by determining the number of degenerating cells positive for Fluoro-Jade B (FJB+) in the region. Compared with age-matched control, greater number of FJB + cells was present per brain section of P14, P28 and adult hypoglycemia groups (P<0.005, each). The cerebral cortex was more vulnerable than hippocampus and striatum at all three ages (P<0.01). Compared with P28 (131±21) and adult (171±21) rats, fewer FJB+ cells (39±6) per brain section were present in P14 hypoglycemic rats (P<0.01, each). Hypoglycemia was not associated with cell injury in P7 rats. FJB+ cells were absent in the hypothalamus in all four ages. Similar results were present 24 hr post-hypoglycemia, where as analysis at 1 wk demonstrated efficient clearing of FJB + cells in the brain regions of developing rats. Varying the duration of fasting did not alter the severity of regional cell injury. These results suggest that postnatal age influences the regional vulnerability to hypoglycemia-induced neuronal death in the rat brain.

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Fluoro-Jade: Novel Fluorochromes for Detecting Toxicant-Induced Neuronal Degeneration

Abstract: ABSTRACT

Cited by 233 publications

References 33 publications

Dissociation of the Neurochemical and Behavioral Toxicology of MDMA (‘Ecstasy’) by Citalopram

Dissociation of the Neurochemical and Behavioral Toxicology of MDMA (‘Ecstasy’) by Citalopram

Visualizing Cell Death in Experimental Focal Cerebral Ischemia: Promises, Problems, and Perspectives

Postnatal age influences hypoglycemia-induced neuronal injury in the rat brain

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