Quinolinic acid: a pathogen in seizure disorders?
Quinolinic acid: a pathogen in seizure disorders?
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喹啉酸：癫痫病的病原体？
DOI：
10.1007/978-1-4684-7971-3_53
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发表时间：
1986
影响因子：
--
通讯作者：
Köhler,C
中科院分区：
文献类型：
--
作者：
Schwarcz,R;Speciale,C;Okuno,E;French,ED;Köhler,C
多行实验证据，在这卷书的几个章节中举例说明，指出大脑N-甲基-D-天冬氨酸(NMDA)受体在癫痫现象中的显著参与，如果不一定是致因的话。目前，这种情况让人想起精神分裂症研究中遇到的情况，在精神分裂症研究中，多巴胺受体似乎以某种方式参与了精神症状学(Snyder等人，1974)。因此，尽管在这两个看似完全不相关的领域进行研究的理论框架非常相似，但存在着一个相当大的差异：多巴胺受体的内源性激动剂的身份是毫无疑问的。事实上，儿茶酚胺为精神分裂症的“多巴胺假说”起了个名字。相比之下，没有出现类似显着性的内源性NMDA激动剂，这可能被普遍接受为人类癫痫疾病的病原体候选。然而，考虑到NMDA的非内源性性质以及谷氨酸对NMDA型兴奋性氨基酸受体亚型的明显非选择性，这种内源性化合物的特征是显著相关的(Foster和Fagg，1984)。在这里，我们将回顾越来越多的证据表明喹啉酸(吡啶2，3-二羧酸；Quin)可能起到这种作用。
Multiple lines of experimental evidence, exemplified in several chapters of this volume, point to a prominent if not necessarily causative involvement of brain N-methyl-D-aspartate (NMDA) receptors in seizure phenomena. At the present time, the situation is reminiscent of that encountered in schizophrenia research where it appears that dopamine receptors are ‘somehow’ involved in psychiatric symptomatology (Snyder et al., 1974). While the theoretical framework for studies in those two seemingly quite unrelated areas is thus remarkably similar, one considerable difference exists: there is no question as to the identity of the endogenous agonist of the dopamine receptor. In fact, the catecholamine has lent its name to the ’dopamine hypothesis’ of schizophrenia. In contrast, no endogenous NMDA-agonist of similar prominence has emerged, which could be generally accepted as a candidate for a pathogen in human epileptic disorders. Yet the characterization of such an endogenous compound is eminently relevant, given the non-endogenous nature of NMDA and the apparent non-selectivity of glutamate for the NMDA-subtype of excitatory amino acid receptors (Foster and Fagg, 1984). Here we will review the growing body of evidence suggesting that quinolinic acid (pyridine 2,3-dicarboxylic acid; QUIN) may fulfill such a role.