Xenon prevents inflammation-induced delayed pain hypersensitivity in rats

Bessière, Baptiste; Laboureyras, Emilie; Laulin, Jean‐Paul; Simonnet, Guy

doi:10.1097/wnr.0b013e328340d7f6

Cited by 7 publications

(3 citation statements)

References 22 publications

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“…B). The dose was chosen based on previous experiments in pain and the knowledge that the anesthetic dose in rats is 161% . This dose decreased axial, limb, and orofacial (ALO) AIMs, with a peak effect at 30 and 60 minutes ( P < 0.01; Fig.…”

Section: Resultsmentioning

confidence: 99%

Inhaling xenon ameliorates l‐dopa‐induced dyskinesia in experimental parkinsonism

Baufreton

Milekovic

et al. 2018

Movement Disorders

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Parkinson's disease motor symptoms are treated with levodopa, but long‐term treatment leads to disabling dyskinesia. Altered synaptic transmission and maladaptive plasticity of corticostriatal glutamatergic projections play a critical role in the pathophysiology of dyskinesia. Because the noble gas xenon inhibits excitatory glutamatergic signaling, primarily through allosteric antagonism of the N‐methyl‐d‐aspartate receptors, we aimed to test its putative antidyskinetic capabilities. We first studied the direct effect of xenon gas exposure on corticostriatal plasticity in a murine model of levodopa‐induced dyskinesia We then studied the impact of xenon inhalation on behavioral dyskinetic manifestations in the gold‐standard rat and primate models of PD and levodopa‐induced dyskinesia. Last, we studied the effect of xenon inhalation on axial gait and posture deficits in a primate model of PD with levodopa‐induced dyskinesia. This study shows that xenon gas exposure (1) normalized synaptic transmission and reversed maladaptive plasticity of corticostriatal glutamatergic projections associated with levodopa‐induced dyskinesia, (2) ameliorated dyskinesia in rat and nonhuman primate models of PD and dyskinesia, and (3) improved gait performance in a nonhuman primate model of PD. These results pave the way for clinical testing of this unconventional but safe approach. © 2018 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

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Section: Resultsmentioning

confidence: 99%

Inhaling xenon ameliorates l‐dopa‐induced dyskinesia in experimental parkinsonism

Baufreton

Milekovic

et al. 2018

Movement Disorders

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“…[40][41][42] In several types of organ injury models, xenon has been shown to exert anti-inflammatory effects 43,44 and decrease neuronal dysfunction associated with neuroinflammation. 45,46 Induction of hypoxia-inducible factor 1alpha (HIF-1a)…”

Section: Modulation Of Neuroinflammationmentioning

confidence: 99%

Preclinical neuroprotective actions of xenon and possible implications for human therapeutics: a narrative review

Maze

2015

Can J Anesth/J Can Anesth

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“…Ketamine pretreatment partially blocks naloxone-precipitated hyperalgesia in fentanyl-treated rats (Laulin et al, 2002) and fentanyl enhancement of carrageenan-induced hyperalgesia (Richebé et al, 2005;Rivat et al, 2002). In the same model, ketamine, BN2572 (a NMDA antagonist) and N 2 O (a gas with anti-NMDA properties) also prevent stress-induced hyperalgesia (Bessière et al, 2007(Bessière et al, , 2010Rivat et al, 2007). Exaggerated hyperalgesia in pre-stressed rats is in part prevented by NMDA antagonists ketamine and BN2572 (Le Roy et al, 2011).…”

Section: N-methyl-d-aspartate (Nmda) Receptormentioning

confidence: 99%

Behavioral characterization, potential clinical relevance and mechanisms of latent pain sensitization

Gerum¹,

Simonin²

2022

Pharmacology & Therapeutics

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Chronic pain is a debilitating disorder that can occur as painful episodes that alternates with bouts of remission and occurs despite healing of the primary insult. Those episodes are often triggered by stressful events. In the last decades, a similar situation has been evidenced in a wide variety of rodent models (including inflammatory pain, neuropathy and opioid-induced hyperalgesia) where animals develop a chronic latent hyperalgesia that silently persists after behavioral signs of pain resolution. This state, referred as latent pain sensitization, is due to the compensatory activation of antinociceptive systems, such as the opioid system or NPY and its receptors. A transitory phase of hyperalgesia can then be reinstated by pharmacological or genetic blockade of these antinociceptive systems or by submitting animals to acute stress. Those observations reveal that there is a constant endogenous analgesia responsible for chronic pain inhibition that might paradoxically contribute to maintain this maladaptive state and could then participate to the transition from acute to chronic pain. Thus, demonstration of the existence of this phenomenon in humans and a better understanding of the mechanisms by which latent pain sensitization develops and maintains over long periods of time will be of particular interest to help identifying new therapeutic strategies and targets for chronic pain treatment. The present review aims to recapitulate behavioral expression, potential clinical relevance, cellular mechanisms and intracellular signaling pathways involved so far in latent pain sensitization.

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Xenon prevents inflammation-induced delayed pain hypersensitivity in rats

Cited by 7 publications

References 22 publications

Inhaling xenon ameliorates l‐dopa‐induced dyskinesia in experimental parkinsonism

Inhaling xenon ameliorates l‐dopa‐induced dyskinesia in experimental parkinsonism

Preclinical neuroprotective actions of xenon and possible implications for human therapeutics: a narrative review

Behavioral characterization, potential clinical relevance and mechanisms of latent pain sensitization

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