Publications by authors named "Naoyo Motoyama"

We previously demonstrated, using a DNA microarray analysis, the down-regulated expression of the slc30a1 gene (zinc transporter 1, ZnT1) in a neuropathic pain model induced by partial sciatic nerve ligation (PSNL). Zinc is an essential trace mineral that plays important roles in physiological functions, and ZnT1 modulates intracellular zinc levels. In the present study, we examined the effects of the down-regulation of the ZnT1 gene in the spinal cord on tactile allodynia.

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Background: Recent studies have revealed the antinociceptive effects of glycine transporter (GlyT) inhibitors in neuropathic pain models such as sciatic nerve-injured and diabetic animals. Bone cancer can cause the most severe pain according to complex mechanisms in which a neuropathic element is included. Bone cancer modifies the analgesic action of opioids and limits their effectiveness, and thus novel medicament for bone cancer pain is desired.

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Bone cancer pain is the most severe among cancer pain and is often resistant to current analgesics. Thus, the development of novel analgesics effective at treating bone cancer pain are desired. Platelet-activating factor (PAF) receptor antagonists were recently demonstrated to have effective pain relieving effects on neuropathic pain in several animal models.

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Injury to peripheral or spinal nerves following either trauma or disease has several consequences including the development of neuropathic pain. This syndrome is often refractory against conventional analgesics; and thus, novel medicaments are desired for its treatment. Recent studies have emphasized that dysfunction of inhibitory neuronal regulation of pain signal transduction may be relevant to the development of neuropathic pain.

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Article Synopsis
  • Neuropathic pain doesn't respond well to traditional painkillers, highlighting the need for new treatments that target glycinergic neurons in the spinal cord, which are involved in pain regulation.
  • Two types of glycine transporters (GlyT1 and GlyT2) in glial cells and neurons can influence how pain signals are processed, and inhibiting these transporters showed promising antiallodynia effects in various neuropathic pain models in mice.
  • The study suggests timing is crucial for medication, as manipulating glycinergic activity can either help or hinder pain management, especially within the critical period right after nerve injury.
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