Fejes-Szabó Annamária, Bohár Zsuzsanna, Vámos Enikő, Nagy-Grócz Gábor, Tar Lilla, Veres Gábor, Zádori Dénes, Szentirmai Márton, Tajti János, Szatmári István, Fülöp Ferenc, Toldi József, Párdutz Árpád, Vécsei László
Department of Neurology, Faculty of Medicine, Albert Szent-Györgyi Clinical Centre, University of Szeged, Semmelweis u. 6, 6725, Szeged, Hungary.
J Neural Transm (Vienna). 2014 Jul;121(7):725-38. doi: 10.1007/s00702-013-1146-2. Epub 2014 Jan 3.
The systemic administration of nitroglycerine induces attacks in migraineurs and is able to activate and sensitize the trigeminal system in animals involving glutamate and α7-nicotinic acetylcholine receptors, among others. Kynurenic acid is one of the endogenous glutamate receptor antagonists, and exerts inhibitory action on the α7-nicotinic acetylcholine receptors. Since kynurenic acid penetrates the blood-brain barrier poorly, therefore a newly synthesized kynurenic acid amide, N-(2-N-pyrrolidinylethyl)-4-oxo-1H-quinoline-2-carboxamide hydrochloride (KYNAa) was used with such a side-chain substitution to facilitate brain penetration in our study. We evaluated its modulatory effect on kynurenic acid concentration in the cervical part of trigemino-cervical complex (C1-C2) and in the model of nitroglycerine-induced trigeminal activation using male Sprague-Dawley rats. One hour after 1 mmol/kg bodyweight KYNAa administration, the kynurenic acid level increased significantly in C1-C2, which returned to the basal level at 300 min measured by high-performance liquid chromatography. KYNAa pre-treatment had dose-dependent, mitigating action on nitroglycerine-induced decrease in calcitonin gene-related peptide and increase in c-Fos, neuronal nitric oxide synthase and calmodulin-dependent protein kinase II alpha expression in the C1-C2. KYNAa also mitigated the behavioural changes after nitroglycerine. Thus, in this model KYNAa is able to modulate in a dose-dependent manner the changes in neurochemical markers of activation and sensitization of the trigeminal system directly and indirectly--via forming kynurenic acid, possibly acting on peripheral and central glutamate or α7-nicotinic acetylcholine receptors. These results suggest that application of kynurenic acid derivatives could be a useful therapeutic strategy in migraine headache in the future with a different mechanism of action.
硝酸甘油的全身给药会诱发偏头痛患者发作,并能激活和致敏动物的三叉神经系统,其中涉及谷氨酸和α7-烟碱型乙酰胆碱受体等。犬尿喹啉酸是内源性谷氨酸受体拮抗剂之一,对α7-烟碱型乙酰胆碱受体具有抑制作用。由于犬尿喹啉酸很难穿透血脑屏障,因此在我们的研究中使用了一种新合成的犬尿喹啉酸酰胺,即N-(2-N-吡咯烷基乙基)-4-氧代-1H-喹啉-2-甲酰胺盐酸盐(KYNAa),通过这种侧链取代来促进其脑内渗透。我们使用雄性Sprague-Dawley大鼠,评估了其对三叉神经颈复合体(C1-C2)颈部犬尿喹啉酸浓度以及硝酸甘油诱导的三叉神经激活模型的调节作用。给予1 mmol/kg体重的KYNAa 1小时后,C1-C2中的犬尿喹啉酸水平显著升高,通过高效液相色谱法在300分钟时测量其恢复到基础水平。KYNAa预处理对硝酸甘油诱导的C1-C2中降钙素基因相关肽减少以及c-Fos、神经元型一氧化氮合酶和钙调蛋白依赖性蛋白激酶IIα表达增加具有剂量依赖性的缓解作用。KYNAa还减轻了硝酸甘油后的行为变化。因此,在该模型中,KYNAa能够通过形成犬尿喹啉酸,可能作用于外周和中枢谷氨酸或α7-烟碱型乙酰胆碱受体,以剂量依赖性方式直接和间接调节三叉神经系统激活和致敏的神经化学标志物变化。这些结果表明,犬尿喹啉酸衍生物的应用可能是未来偏头痛治疗的一种有用策略,其作用机制不同。