Involvement of ryanodine receptors in tetanic sciatic stimulation‐induced long‐term potentiation of spinal dorsal horn and persistent pain in rats

Lü, Nonghua; Cheng, Longzhen; Zhang, Yu‐Qiu; Lü, B.-C.; Li, Yunqing

doi:10.1002/jnr.22799

Cited by 10 publications

(5 citation statements)

References 49 publications

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“…Increasing evidence has shown that the synaptic plasticity of dorsal horn neurons contributes to pain hypersensitivity after noxious stimulation 15 16 . Additionally, noxious stimulation of the sciatic nerve induces long-term potentiation of C-fiber-evoked field potentials in the spinal dorsal horn and leads to persistent pain 17 . Several intracellular signaling pathway and protein kinase cascades mediate the formation of synaptic plasticity of dorsal horn neurons after noxious stimulation 18 .…”

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confidence: 99%

Inhibition of the Rho/Rho kinase pathway prevents lipopolysaccharide-induced hyperalgesia and the release of TNF-α and IL-1β in the mouse spinal cord

Wang

Song

Zhang

et al. 2015

Sci Rep

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Administration of lipopolysaccharide (LPS) by various routes produces profound inflammatory pain hypersensitivity. However, the molecular events that induce this response remain largely uncharacterized. In the present study, we sought to elucidate the role of the Rho/Rho kinase (ROCK) pathway in the release of tumor necrosis factor-α (TNF-α) and interleukin 1β (IL-1β) following injection of LPS into the mouse paw, which is associated with nociceptive behavior. The spinal cord of LPS-treated mice showed increased active GTP-bound RhoA and upregulation of ROCK2 and c-fos compared to the normal saline group. Furthermore, the inflammation-related cytokines TNF-α and IL-1β were markedly increased in the spinal dorsal horn after intraplantar injection of LPS. However, the latter effects were prevented by prophylactic intrathecal administration of the Rho inhibitor (C3 exoenzyme) or the ROCK inhibitor (Y27632). Collectively, our results suggest that the Rho/ROCK signaling pathway plays a critical role in LPS-induced inflammatory pain and that this pathway is coincident with the release of the pro-nociceptive cytokines TNF-α and IL-1β, which produces hyperalgesia.

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confidence: 99%

Inhibition of the Rho/Rho kinase pathway prevents lipopolysaccharide-induced hyperalgesia and the release of TNF-α and IL-1β in the mouse spinal cord

Wang

Song

Zhang

et al. 2015

Sci Rep

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“…Previous reports have shown that neuronal cell stimulation promotes Ca 2+ entry mediated by voltage or agonist-activated plasma membrane Ca 2+ channels; through CICR the resulting cytoplasmic Ca 2+ signals stimulate Ca 2+ release from the ER, amplifying the initial signal and triggering neuronal responses necessary for processes involved in memory and learning (Balschun, 1999 ; Shimuta et al, 2001 ; Galione and Churchill, 2002 ; Mellentin et al, 2007 ; Galeotti et al, 2008 ; Adasme et al, 2011 ; Baker et al, 2011 ; Lü et al, 2012 ; Hopp et al, 2014 ). Here, we report that spatial memory consolidation produced a significant increase in RyR2 mRNA and protein contents when tested 3 days after the end of training; these levels were increased even after 10 or 19 days after training, albeit at these later times the RyR2 increments did not reach significance.…”

Section: Discussionmentioning

confidence: 99%

Long-term potentiation and spatial memory training stimulate the hippocampal expression of RyR2 calcium release channels

Valdés-Undurraga

Lobos

Sánchez-Robledo

et al. 2023

Front. Cell. Neurosci.

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Introduction: Neuronal Ca2+ signals generated through the activation of Ca2+-induced Ca2+ release in response to activity-generated Ca2+ influx play a significant role in hippocampal synaptic plasticity, spatial learning, and memory. We and others have previously reported that diverse stimulation protocols, or different memory-inducing procedures, enhance the expression of endoplasmic reticulum-resident Ca2+ release channels in rat primary hippocampal neuronal cells or hippocampal tissue.Methods and Results: Here, we report that induction of long-term potentiation (LTP) by Theta burst stimulation protocols of the CA3-CA1 hippocampal synapse increased the mRNA and protein levels of type-2 Ryanodine Receptor (RyR2) Ca2+ release channels in rat hippocampal slices. Suppression of RyR channel activity (1 h preincubation with 20 μM ryanodine) abolished both LTP induction and the enhanced expression of these channels; it also promoted an increase in the surface expression of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunits GluR1 and GluR2 and caused a moderate but significant reduction of dendritic spine density. In addition, training rats in the Morris water maze induced memory consolidation, which lasted for several days after the end of the training period, accompanied by an increase in the mRNA levels and the protein content of the RyR2 channel isoform.Discussion: We confirm in this work that LTP induction by TBS protocols requires functional RyR channels. We propose that the increments in the protein content of RyR2 Ca2+ release channels, induced by LTP or spatial memory training, play a significant role in hippocampal synaptic plasticity and spatial memory consolidation.

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“…Ryanodine receptors (RYRs) main agonist is Ca 2+ itself and they play an important role in the amplification of presynaptic Ca 2+ signals leading to neurotransmitters release [112,113] and have been proposed to participate in pain chronicity both in nociceptive neurons via stimulation of calcium-/CaM-dependent protein kinase CaMKII [114] and in the spinal cord dorsal horn triggering the induction of long-term potentiation at C-fibre synapses [115][116][117].…”

Section: Endoplasmic Reticulum Calcium Releasementioning

confidence: 99%

Calcium Signalling in Breast Cancer Associated Bone Pain

Bortolin

Neto

Lamghari

2022

IJMS

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Calcium (Ca2+) is involved as a signalling mediator in a broad variety of physiological processes. Some of the fastest responses in human body like neuronal action potential firing, to the slowest gene transcriptional regulation processes are controlled by pathways involving calcium signalling. Under pathological conditions these mechanisms are also involved in tumoral cells reprogramming, resulting in the altered expression of genes associated with cell proliferation, metastatisation and homing to the secondary metastatic site. On the other hand, calcium exerts a central function in nociception, from cues sensing in distal neurons, to signal modulation and interpretation in the central nervous system leading, in pathological conditions, to hyperalgesia, allodynia and pain chronicization. It is well known the relationship between cancer and pain when tumoral metastatic cells settle in the bones, especially in late breast cancer stage, where they alter the bone micro-environment leading to bone lesions and resulting in pain refractory to the conventional analgesic therapies. The purpose of this review is to address the Ca2+ signalling mechanisms involved in cancer cell metastatisation as well as the function of the same signalling tools in pain regulation and transmission. Finally, the possible interactions between these two cells types cohabiting the same Ca2+ rich environment will be further explored attempting to highlight new possible therapeutical targets.

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Involvement of ryanodine receptors in tetanic sciatic stimulation‐induced long‐term potentiation of spinal dorsal horn and persistent pain in rats

Cited by 10 publications

References 49 publications

Inhibition of the Rho/Rho kinase pathway prevents lipopolysaccharide-induced hyperalgesia and the release of TNF-α and IL-1β in the mouse spinal cord

Inhibition of the Rho/Rho kinase pathway prevents lipopolysaccharide-induced hyperalgesia and the release of TNF-α and IL-1β in the mouse spinal cord

Long-term potentiation and spatial memory training stimulate the hippocampal expression of RyR2 calcium release channels

Calcium Signalling in Breast Cancer Associated Bone Pain

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