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Neuropathic pain can result from a peripheral or central nervous system lesion and is refractory to analgesic therapy [1-2]. Clinical symptoms commonly include stimulus- independent pain (spontaneous pain) and stimulus-evoked pain (hyperalgesia or allydynia) [2]. Of all symptoms in patients with painful neuropathy, spontaneous pain is the most burdensome [2]. Unfortunately, the behavior of spontaneous pain is more difficult occurred than stimulus-evoked pain. So there are few studies on spontaneous pain.
        The behavior of spontaneous pain was expressed strongly in mSNA rats [3, 25]. Lee DH [3] suggested that spontaneous pain is induced by inflammation, which was evoked by L5 SNL plus the L4 chromic gut loop in mSNA rats. Nerve injury is followed by Wallerian degeneration. A large number of proinflammatory mediators including cytokines, growth factors and proteases, are released from schwann cells, microglia cells and neuron cells [4-5,9]. And the inflammation response is the basis of neuropathic pain. TNF¦Áis the first cytokines that plays a critical role in setting the cytokine network, contributing to macrophage recruitment to inflammatory site[6]. So TNF¦Áappears to play a key role for the induction of neuropathic pain following never injury[7-9]. However, the results are based on studying in stimulus-evoked pain, do not show the effect of TNF¦Áin spontaneous pain.
        The cellular immediate early gene c-fos is transiently induced in numerous cell types by many kinds of stimuli and conditions [10]. While the expression of c-fos is suppressed by various means, the pain behavior could be alleviated in the neuropathic pain rats [11-13]. And the result is also in the inflammatory pain rats [14]. So some people suggest using c-fos as a neural marker of pain [15]. However, as previously described in many other studies, c-fos is not a neural marker of the spontaneous pain [16-17]. Thus the relationship between c-fos and pain is not clear until now.
        Minocycline is a second generation semi-synthetic tetracycline that penetrates well into the central nervous system via blood-brain barrier. And it is a strong anti-inflammatory drug, which is used extensively in the studies of stimulus-evoked pain. And all studies indicated that the inflammatory response was suppressed with minocycline pre-surgery, then the symptoms of stimulus-evoked pain alleviated too [18-21]. Minocycline was able to suppress c-fos expressing in spinal dorsal horn as Cho IK reported [14]. What is minocycline effect on the expression of c-fos and TNF¦Á?
        We verified the effect of TNF¦Áand c-fos in the spontaneous pain with mSNA rats. We also verified that effect of minocycline in the spontaneous pain in our study.

[ Last edited by ·ç·ç1ºÅ on 2008-5-8 at 07:47 ]

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Neuropathic pain can result from a peripheral or central nervous system lesion and is refractory to analgesic therapy [1-2]. Clinical symptoms commonly include stimulus- independent pain (spontaneous pain) and stimulus-evoked pain (hyperalgesia or allydynia) [2]. Of all symptoms in patients with painful neuropathy, spontaneous pain is the most burdensome [2]. Unfortunately,¡° the behaviors of spontaneous pain occur more difficultly  than stimulus-evoked pain.¡± So there are few studies on spontaneous pain.
        The behavior of spontaneous pain was expressed strongly in mSNA rats [3, 25]. Lee DH [3] suggested that spontaneous pain ¡°was¡± induced by inflammation, which was evoked by L5 SNL plus the L4 chromic gut loop in mSNA rats. Nerve injury is followed by Wallerian degeneration. A large number of proinflammatory mediators including cytokines, growth factors and proteases,¡°which¡±are released from schwann cells, microglia cells and neuron cells [4-5,9]. And the inflammation response is the basis of neuropathic pain. TNF¦Á is the first cytokines that ¡°play¡± a critical role in setting the cytokine network, contributing to macrophage recruitment to inflammatory site[6]. So TNF¦Á appears to play a key role for the induction of neuropathic pain following never injury[7-9]. However, the results ¡° base¡± on studying in stimulus-evoked pain, do not show the effect of TNF¦Á in spontaneous pain.
        The cellular immediate early gene c-fos is transiently induced in numerous cell types by many kinds of ¡°stimulis¡± and conditions [10]. While the expression of c-fos is suppressed by various means, the pain behavior could be alleviated in the neuropathic pain rats [11-13]. And the result is also in the inflammatory pain rats [14]. So some people suggest using c-fos as a neural marker of pain [15]. However, as previously described in many other studies, c-fos is not a neural marker of the spontaneous pain [16-17]. Thus the relationship between c-fos and pain is not clear until now.
        Minocycline is a second generation semi-synthetic tetracycline that penetrates well into the central nervous system via blood-brain barrier. And it is a strong anti-inflammatory drug, which is used extensively in the studies of stimulus-evoked pain. And all studies indicated that the inflammatory response was suppressed with minocycline pre-surgery, then the symptoms of stimulus-evoked pain alleviated too [18-21]. Minocycline was able to suppress c-fos expressing in spinal dorsal horn as Cho IK reported [14]. What is ¡°the effect of minocycline¡± on the expression of c-fos and TNF¦Á?
        We verified the effect of TNF¦Á and c-fos in the spontaneous pain with mSNA rats. We also verified that¡° the¡± effect of minocycline in the spontaneous pain in our study.
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5Â¥2008-05-07 21:39:44
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the behavior of spontaneous pain is more difficult occurred than stimulus-evoked pain. So there are few studies on spontaneous pain.

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However, the results are based on studying in stimulus-evoked pain, do not show the effect of TNF¦Áin spontaneous pain.
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