Lombard M C, Weil-Fugazza J, Ries C, Allard M
INSERM U.378 Université Victor Segalen Bordeaux-2, Institut François Magendie, 1 Rue Camille St. Saëns, F33076, Bordeaux Cedex, France.
Brain Res. 1999 Jan 23;816(2):598-608. doi: 10.1016/s0006-8993(98)01242-6.
Using quantitative autoradiography, the effects of acute and chronic inflammation on specific 125I-1DMethyl-FLFQPQRFamide binding were investigated in the rat spinal cord dorsal horn superficial layers, at 6 and 24 h and 2, 4, 6 and 12 weeks after induction of monoarthritis produced by injection of killed Mycobacterium butyricum suspended in Freund adjuvant in one tibio-tarsal joint. Six hours after monoarthritis induction, no modification in specific 125I-1DMethyl-FLFQPQRFamide binding was observed, whereas a significant bilateral increase occurred after 24 h and 2 weeks in L4/L5 dorsal horns, with a return to control values at 4, 6 and 12 weeks. Specific 125I-1DMethyl-FLFQPQRFamide binding was also investigated 24 h after monoarthritis induction in rats submitted 4 days before the induction to spinal cord lesions at the thoracic level (T9-T10). Hemisection of the spinal cord contralateral to the affected ankle prevented the transient bilateral increase in specific 125I-1DMethyl-FLFQPQRFamide binding, whereas total spinal cord section induced a significant bilateral decrease. All of these modifications were restricted to the spinal segments receiving afferent input from the arthritic ankle (L4/L5); no modifications were found at the levels L1 or C6-C8. These data suggest that FLFQPQRFamide is involved in spinal nociceptive processing during sustained peripheral nociceptor activation. The effects of spinal cord lesions in monoarthritic rats indicate that the modifications seen in the FLFQPQRFamide system activity, during sustained peripheral inflammation, depend on afferent fiber activation as well as on supraspinal controls.
采用定量放射自显影技术,在由弗氏佐剂中悬浮的死丁酸分枝杆菌注射至一个胫跗关节诱导单关节炎后的6小时、24小时以及2周、4周、6周和12周,研究了急慢性炎症对大鼠脊髓背角浅层特定的125I-1-甲基-FLFQPQRF酰胺结合的影响。诱导单关节炎6小时后,未观察到特定的125I-1-甲基-FLFQPQRF酰胺结合有改变,而在L4/L5背角,24小时和2周后出现显著的双侧增加,在4周、6周和12周恢复至对照值。还在诱导单关节炎前4天对大鼠进行胸段脊髓损伤(T9-T10),在诱导后24小时研究特定的125I-1-甲基-FLFQPQRF酰胺结合。与患侧踝关节对侧的脊髓半横断可防止特定的125I-1-甲基-FLFQPQRF酰胺结合的短暂双侧增加,而全脊髓横断则导致显著的双侧减少。所有这些改变均局限于接受来自关节炎踝关节传入输入的脊髓节段(L4/L5);在L1或C6-C8水平未发现改变。这些数据表明,FLFQPQRF酰胺在持续的外周伤害感受器激活过程中参与脊髓伤害性信息处理。单关节炎大鼠脊髓损伤的影响表明,在持续的外周炎症期间,FLFQPQRF酰胺系统活性的改变取决于传入纤维激活以及脊髓上控制。