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Descending mechanisms activated by the anterior pretectal nucleus initiate but do not maintain neuropathic pain in rats
Author(s) -
Rossaneis A.C.,
Genaro K.,
Dias Q.M.,
Guethe L.M.,
Fais R.S.,
Del Bel E.A.,
Prado W.A.
Publication year - 2015
Publication title -
european journal of pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.305
H-Index - 109
eISSN - 1532-2149
pISSN - 1090-3801
DOI - 10.1002/ejp.638
Subject(s) - neuropathic pain , medicine , anesthesia , methysergide , hyperalgesia , nerve injury , stimulation , (+) naloxone , peripheral nerve injury , sciatic nerve , nociception , opioid , endocrinology , serotonin , receptor
Background The anterior pretectal nucleus ( APtN ) activates descending mechanisms of pain control. This study evaluated whether the APtN also controls neuropathic pain in rats. Methods The hypersensitivity to mechanical stimulation with an electronic v on F rey apparatus and the number of F os‐immunoreactive ( F os‐ir) neurons in the APtN were evaluated in rats before and after chronic 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 (the subsequent 7 days). The injection of 2% lidocaine (0.25 μ L ) or N ‐methyl‐ D ‐aspartate (2.5 μg/0.25 μ L ) into the APtN intensified the tactile hypersensitivity observed 2 days after injury but did not alter the tactile hypersensitivity observed 7 and 14 days after injury. The injection of naloxone (10 ng/0.25 μ L ) or methysergide (40 pg/0.25 μ L ) but not atropine (100 ng/0.25 μ L ) into the APtN also intensified the tactile hypersensitivity observed 2 days after the injury. A significant increase in the number of F os‐ir cells was found in the contralateral APtN 2 days but not 7 or 14 days after the injury. Electrical stimulation of the APtN reduced the 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 serotonergic mediation into the APtN to inhibit hyperalgesia during the initial phase of neuropathic pain.