Xenon-induced changes in CNS sensitization to pain

Adolph, Oliver; Köster, Sarah; Georgieff, Michael; Bäder, S.; Föhr, Karl J.; Kammer, Thomas; Herrnberger, Bärbel; Grön, Georg

doi:10.1016/j.neuroimage.2009.08.034

Cited by 23 publications

(20 citation statements)

References 51 publications

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“…As both processes are NMDA-receptor dependent [11], it is possible that a first treatment with Xe and the ensuing amnestic effect may shift the reconsolidation-extinction boundaries to limit the effectiveness of a second treatment. Xe's rapid on-off kinetics [49] may facilitate its use both in animals and humans as a temporally precise tool to help characterize such transition states and other dynamic memory processes. Given that the timing of interventions aimed at blocking reconsolidation or enhancing extinction may significantly affect treatment outcomes [11], [48], Xe’s rapid kinetics also may enable temporally optimized treatment regimens.…”

Section: Discussionmentioning

confidence: 99%

Xenon Impairs Reconsolidation of Fear Memories in a Rat Model of Post-Traumatic Stress Disorder (PTSD)

et al. 2014

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Xenon (Xe) is a noble gas that has been developed for use in people as an inhalational anesthestic and a diagnostic imaging agent. Xe inhibits glutamatergic N-methyl-D-aspartate (NMDA) receptors involved in learning and memory and can affect synaptic plasticity in the amygdala and hippocampus, two brain areas known to play a role in fear conditioning models of post-traumatic stress disorder (PTSD). Because glutamate receptors also have been shown to play a role in fear memory reconsolidation – a state in which recalled memories become susceptible to modification – we examined whether Xe administered after fear memory reactivation could affect subsequent expression of fear-like behavior (freezing) in rats. Male Sprague-Dawley rats were trained for contextual and cued fear conditioning and the effects of inhaled Xe (25%, 1 hr) on fear memory reconsolidation were tested using conditioned freezing measured days or weeks after reactivation/Xe administration. Xe administration immediately after fear memory reactivation significantly reduced conditioned freezing when tested 48 h, 96 h or 18 d after reactivation/Xe administration. Xe did not affect freezing when treatment was delayed until 2 h after reactivation or when administered in the absence of fear memory reactivation. These data suggest that Xe substantially and persistently inhibits memory reconsolidation in a reactivation and time-dependent manner, that it could be used as a new research tool to characterize reconsolidation and other memory processes, and that it could be developed to treat people with PTSD and other disorders related to emotional memory.

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Section: Discussionmentioning

confidence: 99%

Xenon Impairs Reconsolidation of Fear Memories in a Rat Model of Post-Traumatic Stress Disorder (PTSD)

et al. 2014

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“…For continuous arterial spin labeling (CASL; see Wang et al, 2005 for further technical details) we used the same sequence as reported previously [57]. In brief, the labeling plane was 8 cm beneath the centre of the imaging sections.…”

Section: Methodsmentioning

confidence: 99%

Increased Resting-State Perfusion after Repeated Encoding Is Related to Later Retrieval of Declarative Associative Memories

et al. 2011

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Electrophysiological studies in animals have shown coordinated reactivation of neuronal ensembles during a restricted time period of behavioral inactivity that immediately followed active encoding. In the present study we directly investigated off-line processing of associative memory formation in the human brain. Subjects' regional cerebral blood flow (rCBF) as a surrogate marker of neural activity during rest was measured by MR-based perfusion imaging in a sample of 14 healthy male subjects prior to (Pre2) and after (Post) extensive learning of 24 face-name associations within a selective reminding task (SR). Results demonstrated significant Post-Pre2 rCBF increases in hippocampal and temporal lobe regions, while in a control comparison of two perfusion scans with no learning task in-between (Pre2-Pre1) no differences in rCBF emerged. Post perfusion scanning was followed by a surprise cued associative recall task from which two types of correctly retrieved names were obtained: older names already correctly retrieved at least once during one of the SR blocks, and recent names acquired during the last SR block immediately prior to the Post scan. In the anterior hippocampus individual perfusion increases were correlated with both correct retrievals of older and recent names. By contrast, older but not recently learned names showed a significant correlation with perfusion increases in the left lateral temporal cortex known to be associated with long-term memory. Recent, but not older names were correlated with dopaminergic midbrain structures reported to contribute to the persistence of memory traces for novel information. Although the direct investigation of off-line memory processing did not permit concomitant experimental control, neither intentional rehearsal, nor substantial variations in subjects' states of alertness appear to contribute to present results. We suggest that the observed rCBF increases might reflect processes that possibly contribute to the long-term persistence of memory traces.

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“…These results also suggest that xenon acts at the central level. This hypothesis is reinforced by a recent study showing that xenon-induced changes in CNS sensitization to pain by interfering with synaptic plasticity in the human brain [18].…”

Section: Inflamed Hind Paw (A)mentioning

confidence: 90%

Xenon prevents inflammation-induced delayed pain hypersensitivity in rats

et al. 2010

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Rats received an intraplantar carrageenan injection for inducing hind paw inflammation. After 1 h 45 min, they were exposed to medical air (air group), xenon 25% (Xe-25 group) or 50% (Xe-50 group) for 1 h 45 min. Mechanical nociceptive threshold was evaluated on experimental day and once daily for 1 week. Beyond the well-known antinociceptive effect of xenon, the delayed hyperalgesia observed for 4 days after carrageenan injection was strongly reduced in Xe-25 group and totally suppressed in Xe-50 group on the inflamed hind paw. Moreover, delayed hyperalgesia on the noninflamed hind paw was totally suppressed for both the xenon concentrations. These results show that xenon, beyond its antinociceptive effects, may be a fruitful therapeutic strategy to limit the development of pain sensitization after tissue injury.

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Xenon-induced changes in CNS sensitization to pain

Cited by 23 publications

References 51 publications

Xenon Impairs Reconsolidation of Fear Memories in a Rat Model of Post-Traumatic Stress Disorder (PTSD)

Xenon Impairs Reconsolidation of Fear Memories in a Rat Model of Post-Traumatic Stress Disorder (PTSD)

Increased Resting-State Perfusion after Repeated Encoding Is Related to Later Retrieval of Declarative Associative Memories

Xenon prevents inflammation-induced delayed pain hypersensitivity in rats

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