Involvement of NOX2 in the Development of Behavioral and Pathologic Alterations in Isolated Rats

Schiavone, Stefania; Sorce, Silvia; Dubois‐Dauphin, Michel; Jaquet, Vincent; Colaianna, Marilena; Zotti, Margherita; Cuomo, V.; Trabace, Luigia; Krause, Karl Heinz

doi:10.1016/j.biopsych.2009.04.033

Cited by 194 publications

(217 citation statements)

References 68 publications

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“…These findings are in agreement with [65]. SI increases neuronal oxidative stress [66], which consecutively can stimulate β-and γ-secretase activity [67], resulting in Aβ elevation and cognition deficits, also stress promotes APP processing along the amyloidogenic pathway [65]. Social isolation can also exaggerate the inflammatory processes [68].…”

Section: H5supporting

confidence: 75%

The Role of Mental and Physical Activities against Development of Alzheimer ’s Disease in Socialized and Isolated Rats

Ali¹,

Khalil²,

Elariny³

et al. 2017

Brain Disord Ther

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Section: H5supporting

confidence: 75%

The Role of Mental and Physical Activities against Development of Alzheimer ’s Disease in Socialized and Isolated Rats

Ali¹,

Khalil²,

Elariny³

et al. 2017

Brain Disord Ther

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“…In this context, it has been shown that the activation of the ROS-producing NADPH oxidase NOX2 enzyme contributes to dysfunction of GABAergic interneurons after subchronic ketamine exposure in mice (Behrens et al, 2007(Behrens et al, , 2008. We have also recently demonstrated the involvement of NOX2 in behavioral and biochemical alterations caused by social isolation in rats (Schiavone et al, 2009). These two different animal models induce chronic neural stress and, in both cases, NOX2 upregulation appears to be responsible for the prolonged oxidative insult on GABAergic neurons.…”

Section: Introductionmentioning

confidence: 90%

“…Immunohistochemistry was performed as described previously (Schiavone et al, 2009). Briefly, after deparaffinization and heat-induced epitope retrieval, brain sections were incubated overnight at 4°C with one or two (for double staining) primary antibodies at the following concentrations: 8-hydroxy-2Ј-deoxyguanosine (8-OHdG), 1:10 (JaICA); NMDAR subunit 2A (NMDAR-2A), 1:400 (Abcam); and NMDAR-2B, 1:200 (Abcam).…”

Section: Methodsmentioning

confidence: 99%

The NADPH Oxidase NOX2 Controls Glutamate Release: A Novel Mechanism Involved in Psychosis-Like Ketamine Responses

Sorce¹,

Schiavone²,

Tucci³

et al. 2010

J. Neurosci.

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Subanesthetic doses of NMDA receptor antagonist ketamine induce schizophrenia-like symptoms in humans and behavioral changes in rodents. Subchronic administration of ketamine leads to loss of parvalbumin-positive interneurons through reactive oxygen species (ROS), generated by the NADPH oxidase NOX2. However, ketamine induces very rapid alterations, in both mice and humans. Thus, we have investigated the role of NOX2 in acute responses to subanesthetic doses of ketamine. In wild-type mice, ketamine caused rapid (30 min) behavioral alterations, release of neurotransmitters, and brain oxidative stress, whereas NOX2-deficient mice did not display such alterations. Decreased expression of the subunit 2A of the NMDA receptor after repetitive ketamine exposure was also precluded by NOX2 deficiency. However, neurotransmitter release and behavioral changes in response to amphetamine were not altered in NOX2-deficient mice. Our results suggest that NOX2 is a major source of ROS production in the prefrontal cortex controlling glutamate release and associated behavioral alterations after acute ketamine exposure. Prolonged NOX2-dependent glutamate release may lead to neuroadaptative downregulation of NMDA receptor subunits.

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“…In addition, social isolation increased hippocampal levels of Ab 40 and Ab 42 , which was paralleled by increased b-and g-secretase activities whereas a-secretase activity was unaltered. It is likely that social isolation led to oxidative stress (Schiavone et al, 2009), which in turn stimulated b-and g-secretase activity (Chan et al, 2009) resulting in increased Ab, which then triggered onset of cognition decline in the APP/PS1 mice. These results are consistent with previous reports showing that stress and glucocorticoids similarly promote APP processing along the amyloidogenic pathway (Catania et al, 2009) resulting in the exacerbation of AD-like neuropathology (Billings et al, 2005;Green et al, 2006;Jeong et al, 2006;Srivareerat et al, 2009).…”

Section: Acceleration Of Memory Impairment By Social Isolationmentioning

confidence: 99%

The Involvement of Cdk5 Activator p35 in Social Isolation-Triggered Onset of Early Alzheimer’s Disease-Related Cognitive Deficit in the Transgenic Mice

Hsiao

Chen

et al. 2011

Neuropsychopharmacol

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Epidemiological studies indicate that isolated persons have increased risk of developing Alzheimer's disease (AD). This study investigated the cellular mechanisms of how social isolation influenced amyloid b peptide (Ab) accumulation and affected the severity of AD-associated cognitive decline in a mouse model of AD. Amyloid precursor protein (APP) and presenilin 1 (PS1) double-transgenic (APP/PS1) mice were placed either in isolation or in group from postnatal day 28 and tested for cognitive performance at the age of 3 months with fear-conditioning paradigms. We found that social isolation accelerated impairment of contextual fear memory in the APP/PS1 mice. The magnitude of long-term potentiation in the hippocampal CA1 neurons was significantly lower in the isolated APP/PS1 mice compared with group APP/PS1 and wild-type mice. Hippocampal level of Ab was significantly elevated in the isolated APP/PS1 mice, which was accompanied by an increased calpain activity and p25/p35 ratio. In addition, surface expression of GluR1 subunit of AMPA receptor was decreased by social isolation. The association of p35, and a-CaMKII was significantly less in the isolated APP/PS1 mice indicating that their interaction was impaired. These results suggest that social isolation exacerbates memory deficit by increasing Ab level, leading to the increased calpain activity, conversion of p35 to p25 and decrease in association of p35, a-CaMKII, and GluR1, resulting in the endocytosis of AMPA receptors.

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Involvement of NOX2 in the Development of Behavioral and Pathologic Alterations in Isolated Rats

Cited by 194 publications

References 68 publications

The Role of Mental and Physical Activities against Development of Alzheimer ’s Disease in Socialized and Isolated Rats

The Role of Mental and Physical Activities against Development of Alzheimer ’s Disease in Socialized and Isolated Rats

The NADPH Oxidase NOX2 Controls Glutamate Release: A Novel Mechanism Involved in Psychosis-Like Ketamine Responses

The Involvement of Cdk5 Activator p35 in Social Isolation-Triggered Onset of Early Alzheimer’s Disease-Related Cognitive Deficit in the Transgenic Mice

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