Intracerebroventricular injection of streptozotocin causes neurotoxicity to myelin that contributes to spatial memory deficits in rats

Shoham, Shai; Bejar, Corina; Kovalev, E.; Weinstock, Marta

doi:10.1016/j.expneurol.2003.08.015

Cited by 128 publications

(94 citation statements)

References 37 publications

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“…Cerebral glucose and energy metabolism is associated with oxidative stress. After i.c.v administration, the highest concentration of STZ (3 mg/kg) reaches the fornix and periventricular white matter at the level of 3 rd ventricle, which shows the greatest damage (Shoham et al, 2003) and STZ i.c.v induced memory impairment is independent of its hyperglycemic effect (Mayer et al, 1990). Although the mechanism of action of STZ i.c.v on memory impairment is not yet known, it probably involves the induction of oxidative stress (Feillet-Coudray et al, 1999;Reagan et al, 2000) to which myelin is particularly vulnerable (Smith et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Effects of Erythropoietin on Memory Deficits and Brain Oxidative Stress in the Mouse Models of Dementia

Kumar

Jaggi

Singh

2010

Korean J Physiol Pharmacol

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The present study was undertaken to explore the potential of erythropoietin in memory deficits of mice. Memory impairment was produced by scopolamine (0.5 mg/kg, i.p.) and intracerebroventricular streptozotocin (i.c.v STZ, 3 mg/kg, 10 μl, 1 st and 3 rd day) in separate groups of animals. Morris watermaze test was employed to assess learning and memory. The levels of brain thio-barbituric acid reactive species (TBARS) and reduced glutathione (GSH) were estimated to assess degree of oxidative stress. Brain acetylcholinesterase enzyme (AChE) activity was also measured. Scopolamine/streptozotocin administration induced significant impairment of learning and memory in mice as indicated by marked decrease in Morris water-maze performance. Scopolamine/streptozotocin administration also produced a significant enhancement of brain AChE activity and brain oxidative stress (an increase in TBARS and a decrease in GSH) levels. Treatment of erythropoietin (500 and 1,000 IU/Kg i.p.) significantly reversed scopolamine-as well as streptozotocin-induced learning and memory deficits along with attenuation of those-induced rise in brain AChE activity and brain oxidative stress levels. It may be concluded that erythropoietin exerts a beneficial effect in memory deficits of mice possibly through its multiple actions including potential anti-oxidative effect.

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Section: Discussionmentioning

confidence: 99%

Effects of Erythropoietin on Memory Deficits and Brain Oxidative Stress in the Mouse Models of Dementia

Kumar

Jaggi

Singh

2010

Korean J Physiol Pharmacol

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“…Inflammatory processes and myelin and axonal neurotoxicity has been reported following STZ-icv treatment. Severely affected STZ-icv treated rats had not only astrogliosis, but also extensive cell loss, inferred from the increase in the volume of the ventricular system (Prickaerts et al, 2000;Shoham et al, 2003). Interestingly, one week after a single STZicv 3mg/kg dose, no change in the number or morphology of cholinergic neurons was detected in the basal forebrain nuclei, medial septum, diagonal band or the nucleus basalis magnocellularis and there was no change in the density of cholinergic terminals in the hippocampus (Shoham et al, 2006).…”

Section: Morphologymentioning

confidence: 98%

“…Glial fibrillary acidic protein (GFAP), a marker of astrogliosis, a stereotypic reaction of astrocytes to neuronal damage (Prickaerts et al, 1999), has been found to be increased in both brain homogenates and tissue sections (Prickaerts et al, 1999;2000). Increased GFAP immunocytochemical staining was mainly located in periand paraventricular regions including the septum, fornix and fimbria, striatum and hippocampus, suggesting that altered hippocampal function could result from an impaired innervation and direct damage to this region (Prickaerts et al, 2000;Shoham et al, 2003). Inflammatory processes and myelin and axonal neurotoxicity has been reported following STZ-icv treatment.…”

Section: Morphologymentioning

confidence: 99%

“…STZ-icv administration has been associated with certain brain morphological changes in the brain as early as 1 week following a single drug dose (Shoham et al, 2006), and in both ≥1 year and 4 month old rats (Terwel et al, 1995;Prickaerts et al, 2000;Shoham et al, 2003;2006) (Table 1). Glial fibrillary acidic protein (GFAP), a marker of astrogliosis, a stereotypic reaction of astrocytes to neuronal damage (Prickaerts et al, 1999), has been found to be increased in both brain homogenates and tissue sections (Prickaerts et al, 1999;2000).…”

Section: Morphologymentioning

confidence: 99%

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Central insulin resistance as a trigger for sporadic Alzheimer-like pathology: an experimental approach

Šalković‐Petrišić

Hoyer

2007

Neuropsychiatric Disorders an Integrative Approach

191

135

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SUMMARYA growing body of evidence implicates impairments in brain insulin signaling in early sporadic Alzheimer disease (sAD) pathology. However, the most widely accepted hypothesis for AD aetiology stipulates that pathological aggregations of the amyloid β (Aβ) peptide are the cause of all forms of Alzheimer's disease. Streptozotocinintracerebroventricularly (STZ-icv) treated rats are proposed as a probable experimental model of sAD. The current work reviews evidence obtained from this model indicating that central STZ administration induces brain pathology and behavioural alterations resembling those in sAD patients. Recently, alterations of the brain insulin system resembling those in sAD have been found in the STZ-icv rat model and are associated with tau protein hyperphosphorylation and Aβ-like aggregations in meningeal vessels. In line with these findings the hypothesis has been proposed that insulin resistance in the brain might be the primary event which precedes the Aβ pathology in sAD.4

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“…Previous experiments also reported that there is a direct damage to the septohippocampal system on ICV injection of STZ (Blokland et al, 1993). Oxidative stress that has developed due to ICV injection of STZ (Feillet et al, 1999) known to cause damage to the myelin of neurons which known to be responsible for spatial memory deficits in animal models (Shoham et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of Garcinia Mangostana on Streptozotocin Induced Sporadic Type Alzheimer’s Disease in Mice

Avinash

Reddy²,

Begum

et al. 2016

IJAPSR

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ABSTRACT:Objectives: The main objective of the study is to determine the neuroprotective potential of ethonolic extract of Garcinia mangostana (EEGM) in mouse against IntracerebroventricularStreptozotocin (ICV -STZ) induced sporadic type Alzheimer"s disease. Methods: Neurotoxicity was induced by ICV injection of STZ (0.5 mg/kg/b.w) as a first dose then the second dose after the 48 hours and the animals were pre-treated with ethanolic extract of Garcinia mangostana for 28 days. To assess the behavioral parameters learning and memory, open field and Y-maze were employed. Acetylcholinesterase, antioxidant enzymes (superoxide dismutase, glutathione peroxidise, reduced glutathione and catalase) were estimated in brain tissue. Results: Pre-treatment with EEGM (200 and 400 mg/kg/b.w) exhibited a dose dependent reduction of AChE levels and increased habituation memory and percentage alteration which are indicative of the enhanced cognitive function. The extract showed significant increase in the antioxidant parameter. Conclusion:The study results suggested that the neuroprotective potentiality of EEGM against ICV STZ induced neurotoxicity. The extract of EEGM proved to have a potential therapeutic action in preventing or decreasing the progression of sporadic Alzheimer"s disease due to aging and oxidative stress.

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Intracerebroventricular injection of streptozotocin causes neurotoxicity to myelin that contributes to spatial memory deficits in rats

Cited by 128 publications

References 37 publications

Effects of Erythropoietin on Memory Deficits and Brain Oxidative Stress in the Mouse Models of Dementia

Effects of Erythropoietin on Memory Deficits and Brain Oxidative Stress in the Mouse Models of Dementia

Central insulin resistance as a trigger for sporadic Alzheimer-like pathology: an experimental approach

Neuroprotective Effect of Garcinia Mangostana on Streptozotocin Induced Sporadic Type Alzheimer’s Disease in Mice

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