| Pain was experienced by many people and always produced serious suffering. Pain and hyperalgesia was caused by injury of tissue and peripheral nerves. It is believed that the mechanism leading to hyperalgesia included two aspects. One is the continuous nociceptive input. The other is the change in excitability of neurons in the spinal cord. Many studies in recent years indicated that the activation and translocation of protein kinase C (PKC) of neurons in the dorsal horn of spinal cord was related with hyperalgesia. Activator of PKC such as PMA would result in obvious hyperalgesia and algesia. The reaction induced by formalin injection was blunted and the foot-withdrawal latency to radiant heat stimulation was prolonged after intrathecal H-7, an inhibitor of PKC translocation/activation. Hyperalgesia, however, was not induced after nerve injury in the mice without PKC Y . It is clear that the activation of PKC play an important role in hyperalgesia. Hippocampus is an important part of limibic system, but itsfunction was not declared completely. More studies showed that it was involved inmood, memory and stress, but there were few studies showing the relationship between pain and hippocampus. Recently some experiments indicated hippocampus may be related to pain and hyperalgesia, but how it works is unclear.The aim of the present study is to systematically observe the time-course and distribution of the activation of PKC in the dorsal horn of spinal cord and to study the changes of PKC in hippocampus and distribution in different subfield post-injection of formalin. The results are as follows:1. Increase of protein kinase C immunoreactivity and its time course in spinal cord during inflammation-induced by formalin injection.Forty-two healthy SD rats were divided into 7 groups at random: control, Ih, 3h, 12h, 24h, 3d and 7d group (n=6). The rats in the control group were injected with saline (O.lml). The inflammatory pain and hyperalgesia were induced by subcutaneous injection of 5% formalin solution (O.lml) in the right hind paw, and the tissue of L5 section was obtained in 24h post-injection of saline in control or at different time after formalin injection. In the control, the number of PKC positive cells was rare and the immunoreactive PKC particle distributed in the cytoplasm, nucleus and on or near the cell membrane on average. There is no difference between the two sides(P > 0.05). As compared with control group, there is an increase in thenumber of PKC immunoreactivity positive cells in the dorsal horn of spinal cord after formalin injection. In comparison between the two sides of the dorsal horn, the increases were greater on the injected side than the contralateral side. At the same time, the distribution of was varied accordingly. PKC immunoreactive particle was distributed mainly on the somatotopic neurons, especially on the membrane on the ipsilateral side of the superficial dorsal horn in the lumbar spinal cord. Membrane-bound PKC immunoparticles were increased and distributed on or near the neuron membrane in experimental teams. The nucleus expressed weak or no immunoreactive products(P < 0.05). The increase was obvious in Ih and 24h group, but the increases in 24h were more apparent(P<0.01). The number of PKC positive cells and density returned to the control.The results indicated that during inflammatory pain and hyperalgesia, PKC was activated and translated to membrane, and the immunoreactivity of PKC is increased in the dorsal horn of the spinal cord, and this increase is most obvious in 24h after formalin injection.2. Changes of morphology and protein kinase C immunoreactivity in hippocampal neurons of rat following formalin injectionForty-two SD rats were divided into 7 groups at random: control, Ih, 3h, 12h, Id, 3d and 7d group (n=6). The rats in the control group were injected with saline (O.lml), and thetissue was obtained post-injury 3d. The inflammatory pain and hyperalgesia were induced by subcutaneous injection of 5% formalin solution (O.lml) in t...
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