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https://www.arca.fiocruz.br/handle/icict/16393
DESCENDING MECHANISMS ACTIVATED BY THE ANTERIOR PRETECTAL NUCLEUS INITIATE BUT DO NOT MAINTAIN NEUROPATHIC PAIN IN RATS
Author
Affilliation
Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.
Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.
Oswaldo Cruz Foundation, Fiocruz Rondônia, Porto Velho, RO, Brazil.
Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.
Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.
Department of Morphology, Estomatology and Physiology, Faculty of Odontology of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.
Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.
Oswaldo Cruz Foundation, Fiocruz Rondônia, Porto Velho, RO, Brazil.
Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.
Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.
Department of Morphology, Estomatology and Physiology, Faculty of Odontology of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.
Abstract
Background: The anterior pretectal nucleus (APtN) activates descendingmechanisms of pain control. This study evaluated whether the APtN alsocontrols neuropathic pain in rats.Methods: The hypersensitivity to mechanical stimulation with anelectronic von Frey apparatus and the number of Fos-immunoreactive(Fos-ir) neurons in the APtN were evaluated in rats before and afterchronic constriction injury of the sciatic nerve.Results: The tactile hypersensitivity was characterized by an initial phase(the 2 days following the injury) and a maintenance phase (thesubsequent 7 days). The injection of 2% lidocaine (0.25 μL) orN-methyl-D-aspartate (2.5 μg/0.25 μL) into the APtN intensified thetactile hypersensitivity observed 2 days after injury but did not alter thetactile hypersensitivity observed 7 and 14 days after injury. The injection ofnaloxone (10 ng/0.25 μL) or methysergide (40 pg/0.25 μL) but notatropine (100 ng/0.25 μL) into the APtN also intensified the tactilehypersensitivity observed 2 days after the injury. A significant increase inthe number of Fos-ir cells was found in the contralateral APtN 2 days butnot 7 or 14 days after the injury. Electrical stimulation of the APtN reducedthe tactile hypersensitivity at 2, 7 and 14 days after the nerve ligation.Conclusion: APtN exerts a tonic inhibitory influence on persistent pain.The results point out to an important role of opioid and serotonergicmediation into the APtN to inhibit hyperalgesia during the initial phase ofneuropathic pain.
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