Courteix Christine, Privat Anne-Marie, Pélissier Teresa, Hernandez Alejandro, Eschalier Alain, Fialip Joseph
INSERM, U766, F-63001 Clermont-Ferrand, France.
J Pharmacol Exp Ther. 2007 Sep;322(3):1237-45. doi: 10.1124/jpet.107.123018. Epub 2007 Jun 5.
Agmatine, an endogenous cationic amine resulting from the decarboxylation of L-arginine, produces antihyperalgesic and antiallodynic effects in animal models of chronic neuropathic and inflammatory pain. We examined the effect of agmatine on tactile and thermal allodynia and on mechanical hyperalgesia in streptozocin-induced diabetic rats. To determine its mechanism of action and the potential interest of some of its combinations, the antihyperalgesic effect of agmatine was challenged with alpha(2)-adrenergic imidazoline and opioid-receptor antagonists, and its interaction with the opioid-receptor agonist morphine, the competitive N-methyl-D-aspartate receptor antagonist D-CPP [R(-)-3-(2-carboxypiperazine-4-yl)-propyl-1-phosphonic acid], and the nitric-oxide synthase inhibitor L-NAME (L-N(G)-nitro-L-arginine methyl ester) were examined. When intrathecally (i.t.) injected (4.4 to 438 nmol/rat), agmatine was ineffective in normal rats but suppressed tactile allodynia (von Frey hair test), thermal allodynia (tail immersion test), and mechanical hyperalgesia (paw-pressure test) in diabetic rats. This spinal antihyperalgesic effect was suppressed by idazoxan (40 micromol/rat i.t.) but not by yohimbine (40 micromol/rat i.t.) or naloxone (0.69 micromol/rat i.v.). In diabetic rats, an isobolographic analysis showed that combinations of i.t. agmatine with i.v. L-NAME or with i.t. morphine resulted in an additive antihyperalgesic effect, whereas the agmatine/D-CPP i.t. combination was superadditive. In summary, the present findings reveal that spinal agmatine produces antiallodynic and antihyperalgesic effects in diabetic neuropathic pain involving, at least for its antihyperalgesic effect, the imidazoline receptors. Moreover, agmatine combined with D-CPP produces an antinociceptive synergy in experimental neuropathy, opening opportunities in the development of new strategies for pain therapy.
胍丁胺是一种由L-精氨酸脱羧产生的内源性阳离子胺,在慢性神经性疼痛和炎性疼痛的动物模型中具有抗痛觉过敏和抗异常性疼痛的作用。我们研究了胍丁胺对链脲佐菌素诱导的糖尿病大鼠触觉和热异常性疼痛以及机械性痛觉过敏的影响。为了确定其作用机制以及某些联合用药的潜在价值,我们用α₂-肾上腺素能咪唑啉和阿片受体拮抗剂对胍丁胺的抗痛觉过敏作用进行了挑战,并研究了其与阿片受体激动剂吗啡、竞争性N-甲基-D-天冬氨酸受体拮抗剂D-CPP [R(-)-3-(2-羧基哌嗪-4-基)-丙基-1-膦酸]以及一氧化氮合酶抑制剂L-NAME(L-N(G)-硝基-L-精氨酸甲酯)的相互作用。当鞘内注射(4.4至438 nmol/大鼠)时,胍丁胺对正常大鼠无效,但可抑制糖尿病大鼠的触觉异常性疼痛(von Frey毛发试验)、热异常性疼痛(尾浸试验)和机械性痛觉过敏( paw压力试验)。这种脊髓抗痛觉过敏作用被咪唑克生(40 μmol/大鼠鞘内注射)抑制,但未被育亨宾(40 μmol/大鼠鞘内注射)或纳洛酮(0.69 μmol/大鼠静脉注射)抑制。在糖尿病大鼠中,等效线图分析表明,鞘内注射胍丁胺与静脉注射L-NAME或鞘内注射吗啡联合使用可产生相加的抗痛觉过敏作用,而鞘内注射胍丁胺与D-CPP联合使用则具有超相加作用。总之,目前的研究结果表明,脊髓胍丁胺在糖尿病性神经病理性疼痛中产生抗异常性疼痛和抗痛觉过敏作用,至少就其抗痛觉过敏作用而言,涉及咪唑啉受体。此外,胍丁胺与D-CPP联合使用在实验性神经病变中产生抗伤害感受协同作用,为疼痛治疗新策略的开发提供了机会。