Yezierski P R, Liu S, Ruenes L G, Kajander J K, Brewer L K
The Miami Project, University of Miami, 1600 NW, 10th Avenue, R-48 Miami, FL 33126, USA Department of Neurological Surgery, University of Miami, Miami, FL 33136, USA Department of Anatomy and Cell Biology, University of Miami, Miami, FL 33136, USA Department of Oral Science, University of Minnesota, Minneapolis, MN 55455, USA.
Pain. 1998 Mar;75(1):141-155. doi: 10.1016/S0304-3959(97)00216-9.
Intraspinal injections of the AMPA-metabotropic receptor agonist quisqualic acid (QUIS) were made in an effort to simulate injury induced elevations of excitatory amino acids (EAAs), a well documented neurochemical change following spinal cord injury (SCI). The progressive pathological sequela associated with QUIS injections closely resembles the cascade of events described following ischemic and traumatic SCI and the pathogenesis of cavities in the clinical condition of post-traumatic syringomyelia. Using different injection parameters, i.e. depth and volume, to deliver QUIS into the cord the results have shown that the technique of intraspinal injection can be used to produce graded patterns of neuronal loss in specific regions of the spinal gray matter. Furthermore, neuronal loss in the dorsal horn, sparing the superficial laminae, results in the onset of spontaneous (excessive grooming behavior) and evoked (mechanical allodynia and thermal hyperalgesia) behaviors commonly associated with experimental models of chronic neuropathic pain. Thus, the present results provide a morphological correlate of spontaneous and evoked pain related behaviors following excitotoxic SCI. The behavioral characteristics combined with the similarities between QUIS induced injury and the clinical pathology of SCI support the use of the excitotoxic model in studies related to the central mechanism(s) of altered sensation, including pain, following spinal injury.
向脊髓内注射AMPA-促代谢型受体激动剂喹啉酸(QUIS),旨在模拟损伤诱导的兴奋性氨基酸(EAA)升高,这是脊髓损伤(SCI)后一种有充分文献记载的神经化学变化。与喹啉酸注射相关的进行性病理后遗症与缺血性和创伤性脊髓损伤后所描述的一系列事件以及创伤后脊髓空洞症临床状况下空洞的发病机制极为相似。通过使用不同的注射参数,即深度和体积,将喹啉酸注入脊髓,结果表明脊髓内注射技术可用于在脊髓灰质特定区域产生分级的神经元丢失模式。此外,背角神经元丢失,但浅层板层未受影响,导致出现通常与慢性神经性疼痛实验模型相关的自发行为(过度梳理行为)和诱发行为(机械性异常性疼痛和热痛觉过敏)。因此,本研究结果为兴奋性毒性脊髓损伤后自发和诱发的疼痛相关行为提供了形态学关联。行为特征以及喹啉酸诱导损伤与脊髓损伤临床病理学之间的相似性,支持在与脊髓损伤后包括疼痛在内的感觉改变的中枢机制相关研究中使用兴奋性毒性模型。