Brain research
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The emotional component of nociception is seldom distinguished from pain behavioral testing. The aim of the present study was to develop a behavioral test that indicates the emotional pain responses using the classical conditioning paradigm. The role of the anterior cingulate cortex (ACC) in the process of this pain conditioning response was also evaluated. ⋯ The association between a neutral stimulus and a noxious stimulus could be demonstrated in a Pavlovian conditioning test in free moving rats. Thus, the conditioned response may be employed as a measure of the emotional component of the nociception. It is also suggested that the ACC may play an important role in mediating this conditioning effect.
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Primary afferent neurons in mammalian dorsal root ganglia (DRGs) normally function as independent sensory communication elements. However, it has recently been shown that most DRG neurons are transiently activated when axons of neighboring neurons of the same ganglion are stimulated repetitively and the cross-depolarization contributes to this mutual cross-excitation. Here, we reported the cross-inhibition of mechanoreceptive information in DRG under peripheral inflammatory condition. ⋯ This interaction was not affected by cutting the dorsal roots at the place close to the recorded DRG. Preapplication of naloxone and yohimbine did not block the interaction. Taken together with previous reports, this intraganglionic cross-talking appears to be mediated by collision of retrograde spread of action potentials, or/and at least in part, by an activity-dependent diffusible excitatory substance released from neuronal somata and/or adjacent axons, and detected by neighboring cell somata.
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The recent development of rodent models of bone cancer pain has started to provide the basis for demonstrating the particular neurochemical and behavioral entity of cancer pain. Behaviourally, both spontaneous pain and hyperalgesia related to mechanical, but not thermal, noxious stimuli have been described in cancer-bearing animals. We have carried out a histological and behavioural study focused on the reactivity to noxious heat in C3H/HeJ mice receiving an intratibial injection of 10(5) NCTC 2472 cells. ⋯ This thermal hyperalgesia was prevented by the systemic administration of morphine (15 mg/kg). Throughout the whole period studied, mice showed signs of spontaneous pain behaviour that reached its maximum 3 weeks after inoculation. In conclusion, we show that the presence of thermal heat hyperalgesia is preceded by an initial opioid-mediated hypoalgesic state, in this murine model of bone cancer pain.
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Comparative Study
Changes in phosphorylation of ERK and Fos expression in dorsal horn neurons following noxious stimulation in a rat model of neuritis of the nerve root.
Mechanical compression and chemical inflammation of the spinal nerve root are considered major sensory pathologies secondary to a lumbar disc herniation. In order to elucidate the dorsal horn responsiveness to noxious stimulation to the peripheral tissue in the neuritis model of the nerve root, we examined extracellular signal-regulated kinase (ERK) phosphorylation and Fos expression in spinal cord dorsal horn neurons. Male Sprague-Dawley rats received hemilaminectomies and the implantation of disc tissue that was obtained from coccygeal intervertebral discs. ⋯ The number of Fos-LI neurons observed when the MEK inhibitor, U0126, was administered was significantly suppressed compared to the DMSO- (vehicle control) administered group. The increase in ERK phosphorylation and Fos expression in the spinal cord dorsal horn neurons indicates that responses/activation by the noxious stimulation applied to the periphery were elevated in spinal cord neurons in this neuritis model of the lumbar nerve root. Moreover, the increase in the Fos expression in the spinal cord dorsal horn may have been the result of the activation of the MAP kinase cascade.
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It has been reported that cerebral ischemia induces Thr286 autophosphorylation and translocation of CaMKIIalpha which targets to and phosphorylates NR2B in hippocampus of rats [Neuroscience 96 (2000) 665; J. Biol. Chem. 275 (2000) 23798]. ⋯ Thirdly, our results indicated the concomitant phosphorylation and dephosphorylation of CaMKII and NR2B following ischemia or longer reperfusion. Moreover, the dissociation of CaMKII from NR2B had the same trend as that of the return of CaMKII to cytosol. All these data imply the close relationships between CaMKII and NR2B during ischemia and reperfusion, namely, CaMKII might act as an amplifier of detrimental cellular calcium signal regulated by NMDA receptors when becoming autophosphorylated and targeting to NR2B; conversely, autophosphorylated CaMKII could modulate NMDA receptor channel properties by phosphorylating NR2B.