ArticlePsychopharmacology2005
Effect of the blockade of mu1-opioid and 5HT2A-serotonergic/alpha1-noradrenergic receptors on sweet-substance-induced analgesia.
Article in Psychopharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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18 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- [Non-pharmaceutical measures, topical analgesics and oral administration of glucose in pain management: Austrian interdisciplinary recommendations on pediatric perioperative pain management].Schmerz (Berlin, Germany) · 2014Guideline
- Trial
- Sweet taste and menthol increase cough reflex thresholds.Pulmonary pharmacology & therapeutics · 2012Trial
- Sweet relief or lasting impacts? Review of neonatal pain and sucrose in developing rodents.Pain reports · 2025Article
- Collaborative action between noradrenergic and serotoninergic systems in peripheral antinociception in mice.Journal of biosciences · 2024Article
- Early-Life Iron Deficiency Persistently Alters Nociception in Developing Mice.The journal of pain · 2023Article
- Acute and Chronic Pain from Facial Skin and Oral Mucosa: Unique Neurobiology and Challenging Treatment.International journal of molecular sciences · 2021Review
- The influence of pain, agitation, and their management on the immature brain.Pediatric research · 2020Review
- Real-Time Accumbal Dopamine Response to Negative Stimuli: Effects of Ethanol.ACS chemical neuroscience · 2019Article
- Antinociceptive and anti-inflammatory effects of ginsenoside Rf in a rat model of incisional pain.Journal of ginseng research · 2018Article
- Adverse Behavioral Changes in Adult Mice Following Neonatal Repeated Exposure to Pain and Sucrose.Frontiers in psychology · 2018Article
- Article
- Review
- Antinociceptive actions of peripheral glucose administration.Pharmacology, biochemistry, and behavior · 2014Article
- Aversive stimulus differentially triggers subsecond dopamine release in reward regions.Neuroscience · 2012Article
- Reinforcer-dependent enhancement of operant responding in opioid-withdrawn rats.Psychopharmacology · 2010Article
- Analgesia accompanying food consumption requires ingestion of hedonic foods.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Sucrose-induced analgesia in mice: role of nitric oxide and opioid receptor-mediated system.Indian journal of pharmacologyArticle
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleSweet-substance-induced analgesia has been widely studied, and the investigation of the neurotransmitters involved in this antinociceptive process is an important way for understanding the involvement of the neural system controlling this kind of antinociception.
objectiveThe aim of this study was to investigate the involvement of opioid and monoaminergic systems in sweet-substance-induced analgesia.
methodsThe present work was carried out in an animal model with the aim of investigating whether acute (24 h) or chronic (14 days) intake of a sweet substance, such as sucrose (250 g/l), is followed by antinociception. Tail withdrawal latencies in the tail-flick test were measured before and immediately after this treatment. Immediately after the recording of baseline values, independent groups of rats were submitted to sucrose or tap-water intake and, after chronic treatment, they were pretreated with intraperitoneal administration of (1) naltrexone at 0.5, 1, 2 or 3 mg/kg; (2) naloxonazine at 5, 10, 20 or 30 mg/kg; (3) methysergide at 0.5, 1, 2 or 3 mg/kg; (4) ketanserin at 0.5, 1, 2 or 3 mg/kg; or (5) physiological saline.
resultsNaltrexone and methysergide at two major doses decreased sweet-substance-induced analgesia after chronic intake of a sweet substance. These effects were corroborated by peripheral administration of naloxonazine and ketanserin.
conclusionsThese data give further evidence for: (a) the involvement of endogenous opioids and a mu1-opioid receptor in the sweet-substance-induced antinociception; (b) the involvement of monoamines and 5HT2A serotonergic/alpha1-noradrenergic receptors in the central regulation of the sweet-substance-produced analgesia.
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Registered trials
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