P物质在脊髓水平痛觉传递与痛觉调制中的双重作用

本文在大鼠脊髓背角观察到微电泳导入P物质可激活那些伤害感受神经元,进一步支持P物质在痛觉传递中的作用。本文还以同样参数导入P物质可明显抑制伤害性反应,横断脊髓背半部仍能产生这种镇痛效应.若事先导入纳洛酮,多数(5/6)不能阻断P物质的效应,而事先导入荷包牡丹碱,则多数(5/6)被阻断,以上结果说明P物质在脊髓也有镇痛效应,推测与有γ-氨基丁酸参与的突触前抑制有关。另外,用对氯苯丙氨酸抑制5-羟色胺合成后,刺激中缝大核仍能抑制背角伤害性反应,且能被事先导入P物质拮抗剂所阻断。因此,P物质有可能参与脊髓痛觉传递的下行性调制。     

DUAL ACTION OF SUBSTANCE P IN NOCICEPTION AND PAIN MODULATION AT SPINAL LEVEL

In the present study, the activation of the nociceptive dorsal horn neurons in rats by iontophoretic substance P (SP) has been observed. Thus, the role of SP in spinal nociception is further identified.In addition, the inhibitory effects of iontophoretic SP on nociceptive response (C response) of dorsal horn neurons can also be observed even in rats that have undergone dorsal half transection of spinal cord. These inhibitory effects can be partially blocked by pretreatment with iontophoretic bicuculline but not by naloxone. It indicates that the SP-induced inhibitory effects on the nociceptive response may be mainly mediated by the presynaptic inhibition in which γ-aminobutyric acid (GABA) may be involved.In view of the fact that the inhibitory effect of stimulation of nucleus raphe magnus (NRM) on the nociceptive response of dorsal horn neurons in rats depleted of 5-HT with parachlorophenylalanine (pCPA) can be significantly blocked by iontophoretie SP-antagonist, it is supposed that SP may be involve