Articles: hyperalgesia.
-
J. Neurosci. Methods · Jun 2007
Pressure application measurement (PAM): a novel behavioural technique for measuring hypersensitivity in a rat model of joint pain.
Chronic joint pain affects physical well being and can lead to severe psychological and social problems, therefore successful long-term management is highly sought-after. No current behavioural measures of pain used in pre-clinical models mimic the clinical dolorimeter, which provides an objective measure of joint hypersensitivity. In this study we aim to use a novel behavioural readout alongside an established measure to mimic the multifactorial measurements taken in the clinic. ⋯ Both PAM and the incapacitance tester detected a reversal of hypersensitivity 1h post-drug administration. Furthermore, the two readouts were highly correlated, and power analysis indicated that PAM was highly reproducible. In conclusion, PAM provides a novel, accurate behavioural tool for detecting a primary mechanical hypersensitivity in a rat model of chronic inflammatory joint pain.
-
Conventional thermonociceptive tests are based on measurement of the latency of nocifensive reactions evoked by constant, suprathreshold heat stimuli. In the present study, a novel, increasing-temperature water bath was developed for determination of the noxious heat threshold temperature of lightly restrained conscious rats. One of the hindpaws of a rat was immersed into the water bath whose temperature was increased from 30 degrees C at a rate of 24 degrees C/min until the animal withdrew its hindpaw from the water. ⋯ Morphine, diclofenac, ibuprofen and paracetamol administered intraperitoneally 20 min after heat injury dose-dependently inhibited the drop of heat threshold with minimum effective doses of 0.3, 0.3, 10 and 30 mg/kg, and ED(50) values of 0.5, 3, 18 and 100 mg/kg, respectively. Thermal hyperalgesia was also decreased by intraplantar treatment with morphine (10 microg), diclofenac (10 microg) or ibuprofen (100 microg). In conclusion, the mild heat injury-induced drop of the noxious heat threshold measured with the increasing-temperature water bath is a novel thermal hyperalgesia model highly sensitive to both opioid and non-opioid analgesics upon systemic or local administration.
-
Noradrenergic locus coeruleus (LC) is involved in pain regulation. We studied whether response properties of LC neurons or coeruleospinal antinociception are changed 10-14 days following development of experimental neuropathy. Experiments were performed in spinal nerve-ligated, sham-operated and unoperated male rats under sodium pentobarbital anesthesia. ⋯ Increased responses of LC neurons to noxious somatic stimulation are likely to promote feedback inhibition of neuropathic hypersensitivity, while the enhanced inhibition of the LC from the amygdala is likely to suppress noradrenergic pain inhibition and promote neuropathic pain. It is proposed that the decreased spinal antinociception induced by direct stimulation of the LC may be explained by pronociceptive changes in the non-noradrenergic systems previously described in peripheral neuropathy. Furthermore, we propose the hypothesis that emotions processed by the amygdala enhance pain due to increased inhibition of the LC in peripheral neuropathy.
-
The role of the cellular prion protein (PrP(c)) in neuronal functioning includes neuronal excitability, cellular adhesion, neurite outgrowth and maintenance. Here we investigated the putative involvement of the PrP(c) function on the nociceptive response using PrP(c) null (Prnp(0/0)) and wild-type (Prnp(+/+)) mice submitted to thermal and chemical models of nociception. PrP(c) null mice were more resistant than wild-type mice to thermal nociception of the tail-flick test. ⋯ In contrast, the same pre-treatment did not alter the formalin response in PrP(c) null mice. These results indicate a role of PrP(c) in the nociceptive transmission, including the thermal tail-flick test and visceral inflammatory nociception (acetic acid-induced abdominal constriction). Our findings show that PrP(c) is involved with a response mediated by inflammation (paw edema) and by visceral conditioning stimuli.
-
Acta Anaesthesiol Taiwan · Jun 2007
Effect of intrathecal NG-nitro-L-arginine methyl ester administration on Fos expression in the spinal dorsal horn in rats following sciatic nerve ligation.
In the available literature, the pro- or antinociceptive role of nitric oxide (NO) is warmly disputed. As a marker of neuronal activation of the central nervous system, Fos expression has been widely used to assess the change in central neuronal activity evoked by peripheral input. In this study, we examined the effect of intrathecal L-NAME, a non-selective nitric oxide synthase (NOS) inhibitor, on nociceptive behavior and spinal Fos expression in rats following chronic constriction injury (CCI) of sciatic nerve, a model of neuropathic pain similar to that observed in clinical setting. ⋯ Spinal Fos expression could be induced by different mechanisms, and it should not regarded as a reliable marker of pain sensation disorders. NO plays an important role in the development of nociception and spinal Fos expression through central sensitization mediated by peripheral nerve injury.