Interleukin-1 beta modulates AMPA receptor expression and phosphorylation in hippocampal neurons

Lai, Aaron Y.; Swayze, Richard D.; El-Husseini, Alaa; Song, Cai

doi:10.1016/j.jneuroim.2006.03.001

Cited by 139 publications

(101 citation statements)

References 42 publications

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“…Interestingly, it seems that changes in GluR1 membrane expression would be mediated by NMDA receptors. Blocking these receptors with APV prevented IL-1β-induced downregulation of GluR1 surface expression [30].…”

Section: A Strong Alteration In Membrane Expressionmentioning

confidence: 95%

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Sildenafil Reduces Neuroinflammation and Restores Spatial Learning in Rats with Hepatic Encephalopathy. Underlying Mechanisms

Hernández‐Rabaza¹,

Agustí²,

Cabrera‐Pastor³

et al. 2016

Journal of Hepatology

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Section: A Strong Alteration In Membrane Expressionmentioning

confidence: 95%

“…Lai et al [30] showed that exposure to IL-1β reduces phosphorylation in Ser831 and membrane expression of GluR1 in hippocampal neurons, and this was prevented by IL-1Ra, an antagonist of IL-1 receptors. Interestingly, it seems that changes in GluR1 membrane expression would be mediated by NMDA receptors.…”

Section: A Strong Alteration In Membrane Expressionmentioning

confidence: 99%

Sildenafil Reduces Neuroinflammation and Restores Spatial Learning in Rats with Hepatic Encephalopathy. Underlying Mechanisms

Hernández‐Rabaza¹,

Agustí²,

Cabrera‐Pastor³

et al. 2016

Journal of Hepatology

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“…IL-1β directly modulates ion channels, enhancing NMDA and AMPA [45,46] and reducing the effectiveness of GABA A [48] , which can change the excitability of neurons and may promote FS generation. So in an integrative way, IL-1β can both enhance and reduce neural excitability (neurotoxic and neuroprotective effects) [66] .…”

Section: Discussionmentioning

confidence: 99%

“…IL-1β down-regulates AMPA receptor expression and phosphorylation in a Ca 2+ -and NMDA-dependent manner in hippocampal neurons [45] .…”

Section: +mentioning

confidence: 99%

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IL-1β: an important cytokine associated with febrile seizures?

Liu

et al. 2012

Neurosci. Bull.

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Febrile seizures (FSs) are the most common convulsions in childhood. Studies have demonstrated a significant relationship between a history of prolonged FSs during early childhood and temporal sclerosis, which is responsible for intractable mesial temporal lobe epilepsy. It has been shown that interleukin-1β (IL-1β) is intrinsically involved in the febrile response in children and in the generation of FSs. We summarize the gene polymorphisms, changes of IL-1β levels and the putative role of IL-1β in the generation of FSs. IL-1β could play a role either in enhancing or in reducing neural excitability. If the enhancing and reducing effects are balanced, an FS does not occur. When the enhancing effect plays the leading role, an FS is generated. A mild imbalance can cause simple FSs while a severe imbalance can cause complex FSs and febrile status epilepticus. Therefore, anti-IL-1β therapy may help to treat FSs.

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Acute systemic inflammation exacerbates neuroinflammation in Alzheimer's disease: IL‐1β drives amplified responses in primed astrocytes and neuronal network dysfunction

López-Rodríguez

Hennessy

Murray

et al. 2021

Alzheimer's & Dementia

122

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Neuroinflammation contributes to Alzheimer's disease (AD) progression. Secondary inflammatory insults trigger delirium and can accelerate cognitive decline. Individual cellular contributors to this vulnerability require elucidation. Using APP/PS1 mice and AD brain, we studied secondary inflammatory insults to investigate hypersensitive responses in microglia, astrocytes, neurons, and human brain tissue. The NLRP3 inflammasome was assembled surrounding amyloid beta, and microglia were primed, facilitating exaggerated interleukin-1β (IL-1β) responses to subsequent LPS stimulation.Astrocytes were primed to produce exaggerated chemokine responses to intrahippocampal IL-1β. Systemic LPS triggered microglial IL-1β, astrocytic chemokines, IL-6, and acute cognitive dysfunction, whereas IL-1β disrupted hippocampal gamma rhythm, all selectively in APP/PS1 mice. Brains from AD patients with infection showed elevated IL-1β and IL-6 levels. Therefore, amyloid leaves the brain vulnerable to secondary inflammation at microglial, astrocytic, neuronal, and cognitive levels, and infection amplifies neuroinflammatory cytokine synthesis in humans. Exacerbation of neuroinflammation to produce deleterious outcomes like delirium and accelerated disease progression merits careful investigation in humans.

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Interleukin-1 beta modulates AMPA receptor expression and phosphorylation in hippocampal neurons

Cited by 139 publications

References 42 publications

Sildenafil Reduces Neuroinflammation and Restores Spatial Learning in Rats with Hepatic Encephalopathy. Underlying Mechanisms

Sildenafil Reduces Neuroinflammation and Restores Spatial Learning in Rats with Hepatic Encephalopathy. Underlying Mechanisms

IL-1β: an important cytokine associated with febrile seizures?

Acute systemic inflammation exacerbates neuroinflammation in Alzheimer's disease: IL‐1β drives amplified responses in primed astrocytes and neuronal network dysfunction

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