ArticleJournal of anesthesia2018
Central noradrenergic activity affects analgesic effect of Neuropeptide S.
Article in Journal of anesthesia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Neuropeptide S pathway in PTSD and neuropsychiatric disorders: A review.Biomolecules & biomedicine · 2025Review
- Roles of orexinergic and noradrenergic neuronal activity in ketamine-induced analgesia: A study using an orexin/ataxin-3 transgenic rat model.Journal of anesthesia and translational medicine · 2024Article
- Roles of Neuropeptide S in Anesthesia, Analgesia, and Sleep.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Pharmacology, Physiology and Genetics of the Neuropeptide S System.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Electroacupuncture Alleviates Pain-Related Emotion by Upregulating the Expression of NPS and Its Receptor NPSR in the Anterior Cingulate Cortex and Hypothalamus.Evidence-based complementary and alternative medicine : eCAM · 2020Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeuropeptide S (NPS) is an endogenous neuropeptide controlling anxiolysis, wakefulness, and analgesia. NPS containing neurons exist near to the locus coeruleus (LC) involved in the descending anti-nociceptive system. NPS interacts with central noradrenergic neurons; thus brain noradrenergic signaling may be involved in NPS-induced analgesia. We tested NPS analgesia in noradrenergic neuron-lesioned rats using a selective LC noradrenergic neurotoxin, N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4).
methodsA total 66 male Sprague-Dawley rats weighing 350-450 g were used. Analgesic effects of NPS were evaluated using hot-plate and tail-flick test with or without DSP-4. The animal allocated into 3 groups; hot-plate with NPS alone intracerebroventricular (icv) (0.0, 1.0, 3.3, and 10.0 nmol), tail-flick NPS alone icv (0.0 and 10.0 nmol), and hot-plate with NPS and DSP-4 (0 or 50 mg/kg ip). In hot-plate with NPS and DSP-4 group, noradrenaline content in the cerebral cortex, pons, hypothalamus, were measured.
resultsNPS 10 nmol icv prolonged hot plate (%MPE) but not tail flick latency at 30 and 40 min after administration. DSP-4 50 mg/kg decreased noradrenaline content in the all 3 regions. The NA depletion inhibited NPS analgesic effect in the hot plate test but not tail flick test. There was a significant correlation between hot plate latency (percentage of maximum possible effect: %MPE) with NPS 10 nmol and NA content in the cerebral cortex (p = 0.017, r
conclusionsNPS analgesia interacts with LC noradrenergic neuronal activity.
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Registered trials
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