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Antinociceptive effects of melatonin in a rat model of post-inflammatory visceral hyperalgesia: a centrally mediated process.
Pain. 2010 Jun; 149(3):555-64.PAIN

Abstract

Previous reports suggest that melatonin may play an important role in visceral nociception and neurogenic inflammation. We aimed to examine the role of melatonin on visceral hypersensitivity and to explore the site of action using a rat model of post-inflammatory visceral hyperalgesia. In all rats, a baseline viscero-motor response (VMR) to graded colorectal distension (CRD; 10-60mmHg) was recorded prior and 1 week following tri-nitrobenzenesulfonic acid (TNBS) induced colonic inflammation. Melatonin (30, 45 or 60mg/kg, ip) was given 20min before testing the VMR in naïve and TNBS-treated rats. Extracellular single-unit recordings were made from CRD-sensitive pelvic nerve afferent (PNA) fibers and lumbosacral (LS) spinal neurons in TNBS-treated animals. The effect of melatonin (60mg/kg) was examined on responses of PNAs and spinal neurons to graded CRD. In separate experiments, luzindole (non-specific MT(1)/MT(2) receptor antagonist) or naltrexone (non-specific opiod receptor antagonist) was injected prior to melatonin. Following TNBS, there was a significant increase in the VMR to CRD compared to baseline. This increase was attenuated by melatonin (60mg/kg) at pressures >20mmHg. The same dose of melatonin had no effect on the VMR in naïve animals. In TNBS-treated rats, melatonin significantly attenuated the responses of CRD-sensitive spinal neurons to CRD, but had no effect in spinal transected rats or PNA fibers. Both luzindole and naltrexone blocked melatonin's effect on the VMR and LS spinal neurons. Results indicate melatonin's antinociceptive effects are not via a peripheral site of action but rather a supra-spinal process linked to the central opioidergic system.

Authors+Show Affiliations

Division of Gastroenterology, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI 53226, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20413219

Citation

Mickle, Aaron, et al. "Antinociceptive Effects of Melatonin in a Rat Model of Post-inflammatory Visceral Hyperalgesia: a Centrally Mediated Process." Pain, vol. 149, no. 3, 2010, pp. 555-64.
Mickle A, Sood M, Zhang Z, et al. Antinociceptive effects of melatonin in a rat model of post-inflammatory visceral hyperalgesia: a centrally mediated process. Pain. 2010;149(3):555-64.
Mickle, A., Sood, M., Zhang, Z., Shahmohammadi, G., Sengupta, J. N., & Miranda, A. (2010). Antinociceptive effects of melatonin in a rat model of post-inflammatory visceral hyperalgesia: a centrally mediated process. Pain, 149(3), 555-64. https://doi.org/10.1016/j.pain.2010.03.030
Mickle A, et al. Antinociceptive Effects of Melatonin in a Rat Model of Post-inflammatory Visceral Hyperalgesia: a Centrally Mediated Process. Pain. 2010;149(3):555-64. PubMed PMID: 20413219.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Antinociceptive effects of melatonin in a rat model of post-inflammatory visceral hyperalgesia: a centrally mediated process. AU - Mickle,Aaron, AU - Sood,Manu, AU - Zhang,Zhihong, AU - Shahmohammadi,Golbon, AU - Sengupta,Jyoti N, AU - Miranda,Adrian, Y1 - 2010/04/21/ PY - 2009/11/16/received PY - 2010/03/18/revised PY - 2010/03/22/accepted PY - 2010/4/24/entrez PY - 2010/4/24/pubmed PY - 2010/12/14/medline SP - 555 EP - 64 JF - Pain JO - Pain VL - 149 IS - 3 N2 - Previous reports suggest that melatonin may play an important role in visceral nociception and neurogenic inflammation. We aimed to examine the role of melatonin on visceral hypersensitivity and to explore the site of action using a rat model of post-inflammatory visceral hyperalgesia. In all rats, a baseline viscero-motor response (VMR) to graded colorectal distension (CRD; 10-60mmHg) was recorded prior and 1 week following tri-nitrobenzenesulfonic acid (TNBS) induced colonic inflammation. Melatonin (30, 45 or 60mg/kg, ip) was given 20min before testing the VMR in naïve and TNBS-treated rats. Extracellular single-unit recordings were made from CRD-sensitive pelvic nerve afferent (PNA) fibers and lumbosacral (LS) spinal neurons in TNBS-treated animals. The effect of melatonin (60mg/kg) was examined on responses of PNAs and spinal neurons to graded CRD. In separate experiments, luzindole (non-specific MT(1)/MT(2) receptor antagonist) or naltrexone (non-specific opiod receptor antagonist) was injected prior to melatonin. Following TNBS, there was a significant increase in the VMR to CRD compared to baseline. This increase was attenuated by melatonin (60mg/kg) at pressures >20mmHg. The same dose of melatonin had no effect on the VMR in naïve animals. In TNBS-treated rats, melatonin significantly attenuated the responses of CRD-sensitive spinal neurons to CRD, but had no effect in spinal transected rats or PNA fibers. Both luzindole and naltrexone blocked melatonin's effect on the VMR and LS spinal neurons. Results indicate melatonin's antinociceptive effects are not via a peripheral site of action but rather a supra-spinal process linked to the central opioidergic system. SN - 1872-6623 UR - https://www.unboundmedicine.com/medline/citation/20413219/Antinociceptive_effects_of_melatonin_in_a_rat_model_of_post_inflammatory_visceral_hyperalgesia:_a_centrally_mediated_process_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304-3959(10)00180-6 DB - PRIME DP - Unbound Medicine ER -