Interleukin-1β enhances NMDA receptor-mediated current but inhibits excitatory synaptic transmission

Yang, Shengmei; Liu, Zhenwei; Lei, Wen; Qiao, Haifa; Zhou, Wenxia; Zhang, Yongxiang

doi:10.1016/j.brainres.2004.11.018

Cited by 87 publications

(59 citation statements)

References 17 publications

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“…Through still unknown mechanisms, glia can be activated after injury and release chemical mediators that modulate neuronal activity and synaptic strength. What is most intriguing is that IL-1␤ signaling may facilitate NMDA receptor (NMDAR) activation in neurons (Viviani et al, 2003;Yang et al, 2005). Despite the increasing amount of evidence for the involvement of glia and related chemicals in persistent pain conditions, very few studies have addressed the mechanisms by which these non-neural elements contribute to CNS activity-dependent neuronal plasticity and behavioral hyperalgesia (Tsuda et al, 2003;Milligan et al, 2004;Tanga et al, 2005;Hains and Waxman, 2006;Zhuang et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Glial–Cytokine–Neuronal Interactions Underlying the Mechanisms of Persistent Pain

Guo

Wang²,

Watanabe³

et al. 2007

J. Neurosci.

437

503

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The emerging literature implicates a role for glia/cytokines in persistent pain. However, the mechanisms by which these non-neural elements contribute to CNS activity-dependent plasticity and pain are unclear. Using a trigeminal model of inflammatory hyperalgesia, here we provide evidence that demonstrates a mechanism by which glia interact with neurons, leading to activity-dependent plasticity and hyperalgesia. In response to masseter inflammation, there was an upregulation of glial fibrillary acidic proteins (GFAPs), a marker of astroglia, and interleukin-1␤ (IL-1␤), a prototype proinflammatory cytokine, in the region of the trigeminal nucleus specifically related to the processing of deep orofacial input. The activated astroglia exhibited hypertrophy and an increased level of connexin 43, an astroglial gap junction protein. The upregulated IL-1␤ was selectively localized to astrocytes but not to microglia and neurons. Local anesthesia of the masseter nerve prevented the increase in GFAP and IL-1␤ after inflammation, and substance P, a prototype neurotransmitter of primary afferents, induced similar increases in GFAP and IL-1␤, which was blocked by a nitric oxide synthase inhibitor

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Section: Introductionmentioning

confidence: 99%

Glial–Cytokine–Neuronal Interactions Underlying the Mechanisms of Persistent Pain

Guo

Wang²,

Watanabe³

et al. 2007

J. Neurosci.

437

503

View full text Add to dashboard Cite

show abstract

“…However, some reports using primary cultured hippocampal neurons indicated that IL-1β increased NMDA-mediated Ca 2+ current (31,32); therefore, the effects of IL-1β on NMDA receptors need to be further studied. In addition to the effects on NMDA receptors, IL-1β also affects brain-derived neurotrophic factor-induced signaling in a p38-dependent manner (29), suggesting that various IL-1β-induced signaling events affect LTP induction.…”

Section: Referencesmentioning

confidence: 99%

<b>Synapse-specific effects of IL-1β on long-term potentiation in the mouse hip</b><b>pocampus </b>

et al. 2017

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Interleukin-1β (IL-1β) is a key molecule in the inflammatory responses elicited during infection and injury. It exerts local effects on synaptic plasticity by binding to IL-1 receptors that are expressed at high levels in the hippocampus. We examined the effects of IL-1β on synaptic plasticity in different hippocampal regions in acute mouse brain slices by measuring long-term potentiation (LTP). IL-1β (1 ng/mL) was applied for 30 min before LTP was induced with high-frequency stimulation (HFS). LTP was significantly impaired by either IL-1β application to the Schaffer collateral-CA1 synapses or the associational/commissural (A/C) fiber-CA3 synapses, which are both dependent on N-methyl-D-aspartate (NMDA) receptor activation. However, mossy fiber-CA3 LTP, which is expressed presynaptically in an NMDA-independent manner, was not impaired by IL-1β. Our results demonstrate that IL-1β exerts variable effects on LTP at different kinds of synapses, indicating that IL-1β has synapse-specific effects on hippocampal synaptic plasticity.The immune system and brain constantly communicate with each other in both sickness and health.

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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%

“…It reduces the frequency of AMPA-dependent spontaneous excitatory postsynaptic currents and miniature excitatory postsynaptic currents [46] but enhances NMDA receptormediated currents [45,46] . Viviani et al found that IL-1 increases NMDA receptor function by activating tyrosine kinases and subsequent NR2A/B subunit phosphorylation [47] .…”

Section: +mentioning

confidence: 99%

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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Interleukin-1β enhances NMDA receptor-mediated current but inhibits excitatory synaptic transmission

Cited by 87 publications

References 17 publications

Glial–Cytokine–Neuronal Interactions Underlying the Mechanisms of Persistent Pain

Glial–Cytokine–Neuronal Interactions Underlying the Mechanisms of Persistent Pain

<b>Synapse-specific effects of IL-1β on long-term potentiation in the mouse hip</b><b>pocampus </b>

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

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