Pain
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Coincident with nociception, both noxious chemical stimulation of the hind paw and chronic constriction injury (CCI) of the sciatic nerve produce an increase in protein kinase C (PKC) translocation in the spinal cord of rats. Noxious stimulus-induced PKC translocation likely depends on glutamate activity at either N-methyl-D-aspartate (NMDA) receptors or group I metabotropic glutamate receptors (mGluR1/5) in the spinal cord dorsal horn. This study compares nociceptive responses to, and the alterations in membrane-associated PKC, induced by noxious chemical stimulation of the hindpaw and CCI of the sciatic nerve, as well as their modulation by both NMDA and mGluR1/5 receptor antagonists. ⋯ In contrast, i.t. treatment with (S)-4CPG failed to significantly affect either nociceptive behaviours in the formalin test or formalin-induced increases in [3H]-PDBu binding in laminae I-II and III-VI of the lumbar spinal cord. On the other hand, i.t. treatment with either MK-801 or (S)-4CPG produced a significant reduction in mechanical and cold hypersensitivity, as well as [3H]-PDBu binding in laminae I-II and III-VI of the lumbar spinal cord, after CCI. These results suggest that while NMDA, but not mGluR1/5, receptors are involved in translocation of PKC and nociception in a model of persistent acute pain, both types of receptors influence the translocation of PKC in dorsal horn and mechanical and cold allodynia in a model of chronic neuropathic pain.
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Protein kinase A (PKA) can play a critical role in the modulation of neuronal excitability. We examined the role of PKA in the modulation of abnormal spontaneous activity (SA) originating from the chronically compressed dorsal root ganglion (CCD). The L(4) and L(5) dorsal root ganglia (DRGs) were compressed by inserting a stainless steel rod into each corresponding intervertebral foramen. ⋯ Sp-cAMPS (500 microM), a specific activator of PKA, increased the discharge rate of SA in all injured units tested, but did not trigger firing in silent neurons. Okadaic acid (0.1 microM), a protein phosphatase inhibitor, and forskolin (1 microM), an adenyl cyclase activator, each significantly increased the discharge rate of SA. These results strongly suggest that PKA modulates the SA in injured DRG neurons with myelinated axons.
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This study examined the relationship between pain self-efficacy beliefs and a range of pain behaviours, as measured by the pain behaviour questionnaire (PBQ), using a prospective design. A heterogeneous sample of 145 chronic pain patients completed sets of questionnaires on four occasions over a nine-month period. ⋯ These findings suggest that pain self-efficacy beliefs are an important determinant of pain behaviours and disability associated with pain, over and above the effects of pain, distress and personality variables. In particular, higher pain self-efficacy beliefs are predictive of reduced avoidance behaviours over an extended period.