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3. Nociceptive responses in melatonin MT2 receptor knockout mice compared to MT1 and double MT1/MT2 receptor knockout mice.

Author

Posa, Luca, Lopez‐Canul, Martha, Rullo, Laura, De Gregorio, Danilo, Dominguez‐Lopez, Sergio, Kaba Aboud, Matthew, Caputi, Francesca Felicia, Candeletti, Sanzio, Romualdi, Patrizia, and Gobbi, Gabriella

Subjects
KNOCKOUT mice, G protein coupled receptors
Abstract

Melatonin, a neurohormone that binds to two G protein‐coupled receptors MT1 and MT2, is involved in pain regulation, but the distinct role of each receptor has yet to be defined. We characterized the nociceptive responses of mice with genetic inactivation of melatonin MT1 (MT1−/−), or MT2 (MT2−/−), or both MT1/MT2 (MT1−/−/MT2−/−) receptors in the hot plate test (HPT), and the formalin test (FT). In HPT and FT, MT1−/− display no differences compared to their wild‐type littermates (CTL), whereas both MT2−/− and MT1−/−/MT2−/− mice showed a reduced thermal sensitivity and a decreased tonic nocifensive behavior during phase 2 of the FT in the light phase. The MT2 partial agonist UCM924 induced an antinociceptive effect in MT1−/− but not in MT2−/− and MT1−/−/MT2−/− mice. Also, the competitive opioid antagonist naloxone had no effects in CTL, whereas it induced a decrease of nociceptive thresholds in MT2−/− mice. Our results show that the genetic inactivation of melatonin MT2, but not MT1 receptors, produces a distinct effect on nociceptive threshold, suggesting that the melatonin MT2 receptor subtype is selectively involved in the regulation of pain responses. [ABSTRACT FROM AUTHOR]

Published
2020
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5. Cannabidiol modulates serotonergic transmission and reverses both allodynia and anxiety-like behavior in a model of neuropathic pain

Author

Ryan J. McLaughlin, Gabriella Gobbi, Sabatino Maione, Martha Lopez-Canul, Matthew Kaba Aboud, Luca Posa, Stefano Comai, Justine P Enns, Danilo De Gregorio, Rafael Ochoa-Sanchez, De Gregorio, Danilo, Mclaughlin, Ryan J., Posa, Luca, Ochoa-Sanchez, Rafael, Enns, Justine, Lopez-Canul, Martha, Aboud, Matthew, Maione, Sabatino, Comai, Stefano, and Gobbi, Gabriella

Subjects
Male, Anxiety, Cannabidiol, Dorsal raphe, Electrophysiology, Pain, Pyridines, Action Potentials, Pharmacology, Piperazines, chemistry.chemical_compound, 0302 clinical medicine, Piperidines, 030202 anesthesiology, Ganglia, Spinal, Allodynia, Neurology, Hyperalgesia, Neuropathic pain, Serotonin Antagonists, medicine.symptom, Capsazepine, medicine.drug, Elevated plus maze, Serotonin, medicine.drug_class, TRPV1, Anxiolytic, 03 medical and health sciences, medicine, Animals, Rats, Wistar, Maze Learning, Swimming, business.industry, Antagonist, Feeding Behavior, Rats, Disease Models, Animal, Lysergic Acid Diethylamide, Anesthesiology and Pain Medicine, chemistry, Exploratory Behavior, Neuralgia, Pyrazoles, Neurology (clinical), Capsaicin, business, 030217 neurology & neurosurgery
Abstract

Clinical studies indicate that cannabidiol (CBD), the primary nonaddictive component of cannabis that interacts with the serotonin (5-HT)1A receptor, may possess analgesic and anxiolytic effects. However, its effects on 5-HT neuronal activity, as well as its impact on models of neuropathic pain are unknown. First, using in vivo single-unit extracellular recordings in rats, we demonstrated that acute intravenous (i.v.) increasing doses of CBD (0.1-1.0 mg/kg) decreased the firing rate of 5-HT neurons in the dorsal raphe nucleus, which was prevented by administration of the 5-HT1A antagonist WAY 100635 (0.3 mg/kg, i.v.) and the TRPV1 antagonist capsazepine (1 mg/kg, i.v.) but not by the CB1 receptor antagonist AM 251 (1 mg/kg, i.v.). Repeated treatment with CBD (5 mg/kg/day, subcutaneously [s.c.], for 7 days) increased 5-HT firing through desensitization of 5-HT1A receptors. Rats subjected to the spared nerve injury model for 24 days showed decreased 5-HT firing activity, mechanical allodynia, and increased anxiety-like behavior in the elevated plus maze test, open-field test, and novelty-suppressed feeding test. Seven days of treatment with CBD reduced mechanical allodynia, decreased anxiety-like behavior, and normalized 5-HT activity. Antiallodynic effects of CBD were fully prevented by capsazepine (10 mg/kg/day, s.c., for 7 days) and partially prevented by WAY 100635 (2 mg/kg/day, s.c., for 7 days), whereas the anxiolytic effect was blocked only by WAY. Overall, repeated treatment with low-dose CBD induces analgesia predominantly through TRPV1 activation, reduces anxiety through 5-HT1A receptor activation, and rescues impaired 5-HT neurotransmission under neuropathic pain conditions.

Published
2019

6. Nociceptive responses in melatonin MT 2 receptor knockout mice compared to MT 1 and double MT 1 /MT 2 receptor knockout mice.

Author

Posa L, Lopez-Canul M, Rullo L, De Gregorio D, Dominguez-Lopez S, Kaba Aboud M, Caputi FF, Candeletti S, Romualdi P, and Gobbi G

Subjects
Animals, Mice, Mice, Knockout, Melatonin genetics, Melatonin metabolism, Nociception, Receptor, Melatonin, MT1 deficiency, Receptor, Melatonin, MT1 metabolism, Receptor, Melatonin, MT2 deficiency, Receptor, Melatonin, MT2 metabolism
Abstract

Melatonin, a neurohormone that binds to two G protein-coupled receptors MT 1 and MT 2, is involved in pain regulation, but the distinct role of each receptor has yet to be defined. We characterized the nociceptive responses of mice with genetic inactivation of melatonin MT 1 (MT 1 -/- ), or MT 2 (MT 2 -/- ), or both MT 1 /MT 2 (MT 1 -/- /MT 2 -/- ) receptors in the hot plate test (HPT), and the formalin test (FT). In HPT and FT, MT 1 -/- display no differences compared to their wild-type littermates (CTL), whereas both MT 2 -/- and MT 1 -/- /MT 2 -/- mice showed a reduced thermal sensitivity and a decreased tonic nocifensive behavior during phase 2 of the FT in the light phase. The MT 2 partial agonist UCM924 induced an antinociceptive effect in MT 1 -/- but not in MT 2 -/- and MT 1 -/- /MT 2 -/- mice. Also, the competitive opioid antagonist naloxone had no effects in CTL, whereas it induced a decrease of nociceptive thresholds in MT 2 -/- mice. Our results show that the genetic inactivation of melatonin MT 2 , but not MT 1 receptors, produces a distinct effect on nociceptive threshold, suggesting that the melatonin MT 2 receptor subtype is selectively involved in the regulation of pain responses., (© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Published
2020
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