Articles: hyperalgesia.
-
Biochem. Biophys. Res. Commun. · May 2012
The critical role of spinal ceramide in the development of partial sciatic nerve ligation-induced neuropathic pain in mice.
Recent observations indicate that peripheral nerve injury induces central sensitization through microglial activation and the release of inflammatory cytokines, resulting in the development of neuropathic pain. However, the underlying mechanisms of this phenomenon remain to be fully elucidated. In this study, we examined the involvement of spinal ceramide, a bioactive lipid, in the development of neuropathic pain induced by partial sciatic nerve ligation (PSL). ⋯ In the von Frey test, intrathecal injection of the ceramide biosynthesis inhibitors Fumonisin B1 and GW4869 at 3h and day 3 after PSL significantly attenuated PSL-induced tactile allodynia. By immunohistochemistry, microglial activation in the dorsal horn was suppressed by Fumonisin B1 and GW4869. Therefore, we conclude that spinal ceramide may play a crucial role in PSL-induced neuropathic pain through the activation of microglia.
-
The mechanisms through which electro-acupuncture (EA) and tricyclic antidepressants produce analgesia seem to be complementary: EA inhibits the transmission of noxious messages by activating supraspinal serotonergic and noradrenergic neurons that project to the spinal cord, whereas tricyclic antidepressants affect pain transmission by inhibiting the reuptake of norepinephrine and serotonin at the spinal level. This study utilized the tail-flick test and a model of post-incision pain to compare the antihyperalgesic effects of EA at frequencies of 2 or 100 Hz in rats treated with intraperitoneal or intrathecal amitriptyline (a tricyclic antidepressant). A gradual increase in the tail-flick latency (TFL) occurred during a 20-min period of EA. ⋯ In contrast, it did not significantly change the intensity of the antihyperalgesic effect of 2-Hz EA. The EA-induced antihyperalgesic effects lasted longer after intraperitoneal or intrathecal amitriptyline than after saline, with this effect of amitriptyline being more evident after 100- than after 2-Hz EA. The synergetic effect of amitriptyline and EA against post-incision pain shown here may therefore represent an alternative for prolonging the efficacy of EA in the management of post-surgical clinical pain.
-
Neuroscience research · May 2012
Absence of mechanical hyperalgesia after exercise (delayed onset muscle soreness) in neonatally capsaicin-treated rats.
Delayed onset muscle soreness (DOMS) appears with some delay after unaccustomed, strenuous exercise, especially after lengthening contraction (LC). It is characterized by tenderness and movement related pain, namely muscular mechanical hyperalgesia. ⋯ In these animals, LC failed to induce muscular mechanical hyperalgesia. mRNA of nerve growth factor (NGF) in the muscle, which plays a pivotal role in maintaining mechanical hyperalgesia, was upregulated in the capsaicin treated animals similar to the vehicle treated animals. These results demonstrate that C-fiber afferents are essential in transmitting the nociceptive information from exercised muscle in DOMS.
-
J. Pharm. Pharmacol. · May 2012
Involvement of inflammation in severe post-operative pain demonstrated by pre-surgical and post-surgical treatment with piroxicam and ketorolac.
Post-operative pain is considered to involve inflammation caused by tissue injury. However, the mechanism and timing of the involvement of inflammation in the post-operative pain remain complicated because they can vary among different types of surgery. In this study a rat incision model was used to investigate how inflammation induced by cyclooxygenases (COXs) is involved in severe post-operative pain. ⋯ These findings suggest the involvement of cyclooxygenases in evoking pain that occurs in the immediate post-operative period, and that an initial suppression of rapid inflammation by treatment with NSAIDs before major surgery plays an important role in the management of severe post-operative pain.
-
Observing other people's pain increases our own reports to painful stimuli, a phenomenon that can be defined as 'compassional hyperalgesia' (CH). This functional magnetic resonance imaging study examined the neural correlates of CH, and whether CH could emerge when exposure to the driving stimulus was subliminal. Subjects received electric somatosensory stimuli while observing images of people undergoing painful or enjoyable somatic sensations, presented during a period allowing or not allowing conscious perception. ⋯ CH appears as a high-order phenomenon needing conscious appraisal of the eliciting visual stimulus, and supported by polymodal areas distinct from the basic Pain Matrix. This suggests that compassion to pain does not result from a mere 'sensory resonance' in pain networks, but rather from an interaction between the output of a first-line processing in the Pain Matrix, and the activity of a high-order network involving multisensory integration (temporo-parietal), encoding of internal states (mid-prefrontal) and short-time memory encoding (dorsolateral prefrontal). The Pain Matrix cannot be considered as an 'objective' correlate of the pain experience in all situations.