ABSTRACT
PURPOSE: To explore the potential mechanisms of glutamate and its receptors in stress-induced hyperalgesia. MATERIALS AND METHODS: The stress-induced hyperalgesia, glutamate and its receptors are listed as key items in the pubmed database and the related articles are searched. RESULTS: Glutamate level is increased under stress and associated with stress-induced hyperalgesia. Moreover, the role of glutamate in stress-induced hyperalgesia depends on its subtypes of its receptors. CONCLUSIONS: Increased glutamate during stress connect with ionotropic glutamate receptors can prompt hyperalgesia, but connect with metabotropic glutamate receptors can inhibit hyperalgesia.
Subject(s)
Central Nervous System/metabolism , Central Nervous System/pathology , Glutamic Acid/metabolism , Hyperalgesia/pathology , Animals , Humans , Hyperalgesia/etiology , Receptors, Glutamate/metabolism , Stress, Psychological/complicationsABSTRACT
Exposure to stress could facilitate or inhibit pain responses (stress-induced hyperalgesia or hypoalgesia, respectively). Fluoxetine is a selective serotonin (5-HT) reuptake inhibitor antidepressant. There have been contradictory reports on whether fluoxetine produces antinociceptive effects. The purpose of this study was to elucidate changes in pain sensitivity after chronic stress exposure, and the effects of fluoxetine on these changes. We measured thermal, mechanical, and formalin-induced acute and inflammatory pain by using the tail-flick, von Frey, and formalin tests respectively. The results showed that rats exposed to chronic stress exhibited thermal and formalin-induced acute and inflammatory hypoalgesia and transient mechanical hyperalgesia. Furthermore, fluoxetine promoted hypoalgesia in thermal and inflammatory pain and induced mechanical hyperalgesia. Our results indicate that the 5-HT system could be involved in hypoalgesia of thermal and inflammatory pain and induce transient mechanical hyperalgesia after stress exposure.
