Intranigral lipopolysaccharide induced anxiety and depression by altered BDNF mRNA expression in rat hippocampus

Hrițcu, Lucian; Gorgan, Lucian

doi:10.1016/j.pnpbp.2014.01.016

Cited by 56 publications

(37 citation statements)

References 50 publications

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“…All these findings support the possibility that inflammation contributes to the development of depression by compromising neuroplasticity via reduction of BDNF. In agreement with this line of thinking, it has been recently reported that intranigral LPS infusion induced an anxious and depressive phenotype in the rat that was associated with decreased hippocampal expression of BDNF (Hritcu and Gorgan, 2014 ).…”

Section: The Impact Of Pro-inflammatory Cytokines On Bdnfsupporting

confidence: 67%

Brain-derived neurotrophic factor: a bridge between inflammation and neuroplasticity

Calabrese

Rossetti

Racagni

et al. 2014

Front. Cell. Neurosci.

404

253

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Cytokines are key regulatory mediators involved in the host response to immunological challenges, but also play a critical role in the communication between the immune and the central nervous system. For this, their expression in both systems is under a tight regulatory control. However, pathological conditions may lead to an overproduction of pro-inflammatory cytokines that may have a detrimental impact on central nervous system. In particular, they may damage neuronal structure and function leading to deficits of neuroplasticity, the ability of nervous system to perceive, respond and adapt to external or internal stimuli. In search of the mechanisms by which pro-inflammatory cytokines may affect this crucial brain capability, we will discuss one of the most interesting hypotheses: the involvement of the neurotrophin brain-derived neurotrophic factor (BDNF), which represents one of the major mediators of neuroplasticity.

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Section: The Impact Of Pro-inflammatory Cytokines On Bdnfsupporting

confidence: 67%

Brain-derived neurotrophic factor: a bridge between inflammation and neuroplasticity

Calabrese

Rossetti

Racagni

et al. 2014

Front. Cell. Neurosci.

404

253

View full text Add to dashboard Cite

show abstract

“…In support with this hypothesis, LPS has been demonstrated to impair longterm potentiation, a key cellular process of learning and memory consolidation [28,29]. It has been previously demonstrated that LPS reduces hippocampal mRNA levels of BDNF, a neurotrophin that plays an important role in learning and memory processes [29]. Furthermore, it is reported that the inhibition of IL-1β signaling through the addition of a soluble IL-1β receptor antagonist fully prevented the synaptic deficit induced by LPS administration [30] In line with these findings, we found that LPS administration caused a reduction in BDNF levels in the hippocampus of mice, while EPO treatment rescued the reduction of BDNF levels.…”

Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 90%

Systemic Lipopolysaccharide Administration-Induced Cognitive Impairments are Reversed by Erythropoietin Treatment in Mice

et al. 2015

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Sepsis-associated encephalopathy (SAE) is a frequent complication in critically ill patients and is associated with long-term cognitive impairments. However, the pathophysiology underlying SAE is poorly understood and the pharmacologic treatment is lacking. The purpose of the present study was to investigate the effects of erythropoietin (EPO) on cognitive impairments in an animal model of SAE induced by peripheral administration of lipopolysaccharide (LPS). Mice were randomly divided into the sham + vehicle, sham + EPO, LPS + vehicle, and LPS + EPO groups. EPO was administrated 30 min after the LPS administration and daily afterward for 2 days. Behavioral tests were performed on days 6 and 7 with open field and fear conditioning tests, respectively. The survival rate was estimated by the Kaplan-Meier method. The levels of proinflammatory responses, oxidative stress, and apoptosis-related markers were measured in the hippocampus at the indicated time points. The synaptic morphometry changes in the CA1 region were observed with transmission electron microscopy. Our results showed that LPS administration resulted in high mortality rate and cognitive impairments, which were accompanied by increased expressions of interleukin-1β, malondialdehyde, cleaved caspase-3, and abnormal synaptic morphometry changes in the hippocampus. Notably, EPO treatment reversed the cognitive impairments and rescued the brain pathology induced by LPS administration. In conclusion, our data suggested that treatment with EPO reduced the mortality rate and ameliorated cognitive impairments in an animal model of SAE.

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“…Given that inflammatory cytokine receptors are highly concentrated in areas associated with learning and memory, particularly in hippocampal regions [4], LPS-induced neuroinflammation in the adult brain may disrupt hippocampus-dependent learning and memory [5,6]. Moreover, recent studies have shown that peripheral LPS administration decreases the expression of BDNF in the hippocampus which contributes to cognitive impairment [1,7]. Therefore, it might be possible to prevent LPS-induced cognitive dysfunction by inhibiting neuroinflammation and increasing BDNF expression.…”

Section: Introductionmentioning

confidence: 99%

Acute nicotine treatment attenuates lipopolysaccharide-induced cognitive dysfunction by increasing BDNF expression and inhibiting neuroinflammation in the rat hippocampus

Wei

Qing-shen

et al. 2015

Neuroscience Letters

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Intranigral lipopolysaccharide induced anxiety and depression by altered BDNF mRNA expression in rat hippocampus

Cited by 56 publications

References 50 publications

Brain-derived neurotrophic factor: a bridge between inflammation and neuroplasticity

Brain-derived neurotrophic factor: a bridge between inflammation and neuroplasticity

Systemic Lipopolysaccharide Administration-Induced Cognitive Impairments are Reversed by Erythropoietin Treatment in Mice

Acute nicotine treatment attenuates lipopolysaccharide-induced cognitive dysfunction by increasing BDNF expression and inhibiting neuroinflammation in the rat hippocampus

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