Quinolinic acid accumulation in injured spinal cord: time course, distribution, and species differences between rat and guinea pig.

Quinolinic acid accumulation in injured spinal cord: time course, distribution, and species differences between rat and guinea pig.
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受损脊髓中喹啉酸的积累:大鼠和豚鼠之间的时间过程、分布和物种差异。

DOI:
10.1089/neu.1997.14.89
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发表时间:
1997
期刊:
Journal of neurotrauma.
影响因子:
--
通讯作者:
Heyes,MP
Heyes,MP
中科院分区:
--
文献类型:
--
作者:
Blight,AR;LeroyJr,EC;Heyes,MP

文献摘要

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豚鼠脊髓实验性压迫损伤导致延迟性神经功能缺损,其严重程度在创伤后数天内持续增加,与炎症反应一致,包括单核吞噬细胞侵袭病变和神经毒素喹啉酸(QUIN)水平升高。大鼠脊髓挫伤后也会出现炎症反应和QUIN升高,但立即出现最大的神经功能缺损。在这项研究中,我们测量了豚鼠和大鼠在类似胸脊髓压迫损伤后的体感诱发电位(SEP)和QUIN的组织、血清和脑脊液水平。SEP变化在不同物种之间有所不同,与其他神经学变化一致。在豚鼠中,损伤部位的QUIN水平在损伤后1天开始升高,在12天达到最大升高(100倍),然后下降,但在损伤后25天仍高于血清水平。脊髓的邻近区域也出现了类似的增加,但峰值水平较低。在大鼠中,病变中心的组织QUIN始终低于血清水平,在7天内适度增加(< 10倍),然后在7天至25天之间下降。这些数据表明豚鼠和大鼠在QUIN积累和神经功能缺损的时间过程和程度上存在差异,这可能与继发性病理机制的差异有关。这种深刻的差异可能会影响这些物种用于评估中枢神经系统炎症性疾病的实验性治疗。关键词:炎症;巨噬细胞;quinolinate;脊髓损伤;体感诱发电位
Experimental compression injury of the spinal cord in guinea pigs results in delayed neurologic deficits that continue to increase in severity for several days following trauma, coincident with inflammatory responses, including invasion of the lesion by mononuclear phagocytes and increased levels of the neurotoxin quinolinic acid (QUIN). Inflammatory responses and QUIN elevation also occur following spinal cord contusion in rats, but maximal neurologic deficits develop immediately. In this study, somatosensory evoked potentials (SEP) and tissue, serum, and cerebrospinal fluid levels of QUIN were measured in guinea pigs and rats following similar compression injuries of the thoracic spinal cord. SEP changes differed between the species, consistent with other neurological changes. In guinea pigs, increases in QUIN levels at the lesion site began at 1 day postinjury, achieved maximal elevation (100-fold) by 12 days, then declined, but remained above serum levels at 25 days postinjury. A similar increase occurred in adjacent areas of the spinal cord, with lower peak levels. In rats, tissue QUIN at the center of the lesion remained below serum levels at all times, increasing moderately (< 10-fold) up to 7 days, then decreasing between 7 and 25 days. These data demonstrate differences in the time course and magnitude of QUIN accumulation and neurological deficit between guinea pig and rat, which may relate to differences in secondary pathological mechanisms. Such profound differences may affect the use of these species for evaluation of experimental therapy in this and other inflammatory conditions of the central nervous system.Key words:inflammation; macrophage; quinolinate; spinal trauma; somatosensory evoked potentials