作者: Mei Xu , Megumi Aita , Charles Chavkin
DOI: 10.1016/J.JPAIN.2008.06.006
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摘要: Abstract Trigeminal nerve damage often leads to chronic pain syndromes including trigeminal neuralgia, a severely debilitating orofacial syndrome. Options for treatment of neuropathic are limited in effectiveness and new approaches based on better understanding the underlying pathologies required. Partial ligation has been shown effectively mimic many qualities human syndromes. We have devised mouse model neuralgia using partial infraorbital (pIONL) that induces persistent behaviors morphological changes brainstem. found pIONL induced mechanical allodynia lasting more than 3 weeks. Cell proliferation (bromodeoxyuridine), activation astrocytes microglia ipsilateral caudal medulla, satellite cell reaction ganglion were observed. Neurochemical markers calcitonin gene-related peptide, substance P decreased medullary dorsal horn injury side, whereas receptor NK1 expression was increased after 8 days. Nerve marker ATF3 markedly neurons at days pIONL. The data indicate mice produces anatomical pain, as well allodynia. Perspective This study describes development pain. Our goal is devise treatments this will be facilitated by characterization cellular molecular neuropathological mechanisms genetically designed mice.