Potential of sucrose‐induced analgesia to relieve pain in male adults: A preliminary study

Kakeda, Takahiro

doi:10.1111/j.1742-7924.2010.00150.x

Cited by 12 publications

(16 citation statements)

References 17 publications

(26 reference statements)

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“…[9] In the present study, 12 day ingestion of 32% sucrose solution demonstrated an analgesic effect in mice. This analgesic effect was partially inhibited by long-acting opioid receptor antagonist naltrexone (20 mg/kg), but was unmodified by the NO synthase (NOS) inhibitor L-NAME (10 mg/kg).…”

Section: Discussionsupporting

confidence: 50%

Sucrose-induced analgesia in mice: Role of nitric oxide and opioid receptor-mediated system

et al. 2013

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Background:The mechanism of action of sweet substance-induced analgesia is thought to involve activation of the endogenous opioid system. The nitric oxide (NO) pathway has a pivotal role in pain modulation of analgesic compounds such as opioids.Objectives:We investigated the role of NO and the opioid receptor-mediated system in the analgesic effect of sucrose ingestion in mice.Materials and Methods:We evaluated the effect of intraperitoneal administration of 10 mg/kg of NO synthase inhibitor, N-nitro-L-arginine methyl ester (L-NAME) and 20 mg/kg of opioid receptor antagonist, naltrexone on the tail flick response in sucrose ingesting mice.Results:Sucrose ingestion for 12 days induced a statistically significant increase in the latency of tail flick response which was unmodified by L-NAME, but partially inhibited by naltrexone administration.Conclusions:Sucrose-induced nociception may be explained by facilitating the release of endogenous opioid peptides. Contrary to some previously studied pain models, the NO/cyclic guanosine monophosphate (cGMP) pathway had no role in thermal hyperalgesia in our study. We recommend further studies on the involvement of NO in other animals and pain models.

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Section: Discussionsupporting

confidence: 50%

Sucrose-induced analgesia in mice: Role of nitric oxide and opioid receptor-mediated system

et al. 2013

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“…There is evidence for a more global antinociceptive effect of certain tastants. Sucrose has been reported to elicit antinociception in juveniles (Blass et al, 1987;Miller et al, 1994;Bucher et al, 2000;Anseloni et al, 2005) and in adults (Stevens & Lawless, 1986;Kakeda, 2010;Sch€ obel et al, 2012). Water, sucrose and self-initiated ingestion of chocolate produced analgesia in rats in a manner requiring intact central antinociceptive pathways (Foo & Mason, 2009).…”

Section: Mechanisms and Functional Significance Of Tastant Modulationmentioning

confidence: 99%

Gustatory modulation of the responses of trigeminal subnucleus caudalis neurons to noxious stimulation of the tongue in rats

Boucher

Felizardo

Klein

et al. 2013

Eur J of Neuroscience

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Certain tastants inhibit oral irritation by capsaicin, whereas anesthesia of the chorda tympani (CT) enhances oral capsaicin burn. We tested the hypothesis that tastants activate the CT to suppress responses of trigeminal subnucleus caudalis (Vc) neurons to noxious oral stimuli. In anesthetized rats, we recorded Vc unit responses to noxious electrical, chemical (pentanoic acid, 200 μm) and thermal (55 °C) stimulation of the tongue. Electrically evoked responses were significantly reduced by a tastant mix and individually applied NaCl, monosodium glutamate (MSG), and monopotassium glutamate. Sucrose, citric acid, quinine and water (control) had no effect. Pentanoic acid-evoked responses were similarly attenuated by NaCl and MSG, but not by other tastants. Responses to noxious heat were not affected by any tastant. Transection and/or anesthesia of the CT bilaterally affected neither Vc neuronal responses to electrical or pentanoic acid stimulation, nor the depressant effect of NaCl and MSG on electrically evoked responses. Calcium imaging showed that neither NaCl nor MSG directly excited any trigeminal ganglion cells or affected their responses to pentanoic acid. GABA also had no effect, arguing against peripheral effects of GABA, NaCl or MSG on lingual nocicepive nerve endings. The data also rule out a central mechanism, as the effects of NaCl and MSG were intact following CT transection. We speculate that the effect is mediated peripherally by the release from taste receptor cells (type III) of some mediator(s) other than GABA to indirectly inhibit trigeminal nociceptors. The results also indicate that the CT does not exert a tonic inhibitory effect on nociceptive Vc neurons.

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“…Thus, the analgesic system block pain signals at the initial entry point to the spinal cord. 18,19 The use of different methods for evaluating pain is important because analgesic effect may be due to one or more mechanisms. For this reason in this study we have used hot plate method for supraspinal analgesia and acetic acid induced writhing for spinal analgesia.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of analgesic activity of glucose in Swiss Albino mice

Shobnaarani

Vinotha

et al. 2019

Int J Basic Clin Pharmacol

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Background: Pain is the first and foremost symptom which alerts us about the underlying diseases, injuries or inflammation. Varied treatments are followed for pain relief worldwide. Nowadays tramadol, a centrally acting opioid analgesic is used widely. There are evidences that sweet substances like sucrose produce analgesia through endogenous opioid system. Sucrose has been proved to produce analgesic effect in healthy neonates and also in animals. Likewise, analgesic effect of glucose has also been studied but only limited no. of studies available. Methods: Swiss Albino mice of either sex (20-30g) were procured from the central animal house of KFMS and R, Coimbatore. Animals were maintained under controlled temperature and light conditions with food and water ad libitum. Mice were kept in the department to get acclimatized. 24 mice were divided into 4 groups (n=6). Drugs were given orally after 12hours of fasting. Group I was the control. Group II received standard-tramadol (40mg/kg). Group III received glucose (200mg/kg). Group IV received glucose (400mg/kg). Results: The latency period of glucose was significant (p<0.001) compared to controls and standard was significant (p<0.001) when compared to glucose by hot plate method. Conclusions: Analgesic activity of glucose may be due to both central and peripheral inhibition of PG synthesis. This has been proved in previous studies. This study showed that glucose can be used as an add-on in non-diabetic patients with better compliance.

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Potential of sucrose‐induced analgesia to relieve pain in male adults: A preliminary study

Cited by 12 publications

References 17 publications

Sucrose-induced analgesia in mice: Role of nitric oxide and opioid receptor-mediated system

Sucrose-induced analgesia in mice: Role of nitric oxide and opioid receptor-mediated system

Gustatory modulation of the responses of trigeminal subnucleus caudalis neurons to noxious stimulation of the tongue in rats

Evaluation of analgesic activity of glucose in Swiss Albino mice

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