Pain
-
Comparative Study
Analysis of ultrasonic vocalisation does not allow chronic pain to be evaluated in rats.
Most pain tests used for the assessment of drug analgesic activity in animal chronic pain models are based on the measurement of the response to an external acute stimulation (thermal, mechanical or electrical). But these stimuli are not related to the chronic pain experienced by the animal. Quantitative analysis of the spontaneous behaviour induced by the chronic pain state is needed. ⋯ In a third study, the influence of three parameters, degree of confrontation between the rats, age of the conspecific and housing conditions (isolated or collective) was studied in the arthritic rat model. Arthritic rats did not emit more USVs than controls in any of our experimental conditions. A fourth study showed that Aspirin (200 mg/kg) had no effect on the USVs, this data confirms the lack of direct relationship between USVs and experimental chronic pain in rats in our conditions.
-
The descending colon and rectum are innervated by primary afferent fibers projecting to the lumbosacral and thoracolumbar spinal cord segments. Previous work from this laboratory has suggested that afferent input and sensory processing in the lumbosacral spinal cord is necessary and sufficient to mediate reflex responses to transient colorectal stimulation while processing in both the lumbosacral and thoracolumbar spinal cord segments contribute to visceral hyperalgesia. In the rat, repetitive noxious colorectal distention (CRD) induces >200 Fos labeled cells per section in the lumbosacral segments, but few in the thoracolumbar segments, further suggesting that transient colonic nociceptive input is transduced primarily in the lumbosacral spinal cord. ⋯ Colonic inflammation plus CRD did not significantly increase the percentage of spinoparabrachial neurons that were labeled for Fos compared to distention alone. (4) In the thoracolumbar spinal cord less than 10% of the FG labeled neurons were double labeled for Fos following CRD, but 25% of the FG labeled neurons in the SDH were double labeled following colonic inflammation. These data support the hypothesis that colonic inflammation activates viscerosensory processing in the thoracolumbar spinal cord and further suggests that this information is relayed to the PBn. The increase in information reaching the PBn over these parallel pathways may contribute to the affective-motivational component of the pain experience.
-
Randomized Controlled Trial Multicenter Study Clinical Trial
Intra-articular morphine as analgesic in temporomandibular joint arthralgia/osteoarthritis.
The aim of this study was to determine the analgesic efficacy of a single dose intra-articular injection (i.a.) of morphine in 53 patients with unilateral arthralgia/osteoarthritis of the temporomandibular joint (TMJ). This randomized, double-blind, parallel group, multicenter study included a screening visit, a treatment visit, and a follow-up visit 1 week after treatment. Recordings of visual analog scales (VAS) pain intensity scores at maximum mouth opening (main efficacy variable) and at jaw rest were made directly before a 1-ml i.a. injection into one TMJ of either 1.0mg morphine-HCl, 0.1mg morphine-HCl, or saline (placebo). ⋯ In conclusion, one i.a. injection of 0.1mg morphine significantly increased the pain pressure threshold and mouth opening ability, but evidence for the analgesic property of the locally applied opioid was inconclusive. No dose-effect relation and no significant short-term analgesic property were seen. Although statistically significant, the magnitude of the reduced VAS pain intensity score was not clinically relevant at the 1-week follow-up.
-
A variety of second messenger systems have been implicated in the intracellular mechanisms of tolerance development to the analgesic actions of morphine, a mu opioid, and clonidine, an alpha-2 adrenergic receptor agonist. Here, we studied mice that carry a null mutation in the gene encoding a neuronal specific isoform of protein kinase C (PKC), namely, PKC gamma. We used the tail-flick test to construct dose-response curves before and 4 days after chronic morphine (75-mg pellets, subcutaneously (s.c.)) or clonidine treatment (0.3mg/kg, s.c., twice daily). ⋯ Chronic morphine treatment can also result in sensitization of spinal cord neurons and increased pain behaviors following a noxious insult. To assess the contribution of PKC gamma to this process, we studied the responses of wild-type and mutant mice to an intraplantar injection of formalin (a model of persistent pain) following chronic morphine treatment. Although morphine tolerance increased formalin-evoked persistent pain behavior and Fos-LI in wild-type mice, there was no difference between placebo- and morphine-treated mutant mice, suggesting that PKC gamma also contributes to chronic morphine-induced changes in nociceptive processing.