Sagratella S, Frank C, de Carolis A S
Laboratorio Farmacologia Istituto Superiore di Sanitá, Roma, Italy.
Pharmacol Biochem Behav. 1990 Apr;35(4):999-1001. doi: 10.1016/0091-3057(90)90391-t.
The inhibitory influence of excitatory amino acid (E.A.A.) antagonists such as kynurenic acid, 2-amino-5-phosphonopentanoic acid (AP5), cis-2,3-piperidine dicarboxylic acid (cis-2,3 PDA) and (+)-5-methyl-10,11,-dihydro-5H-dibenzo(a,d)cyclo-hepten-5,10-imine maleate (MK 801), has been studied on the epileptiform activity elicited in rat hippocampal slices, bathed in penicillin (1 mM). The rank of the inhibitory potency was: MK 801 greater than kynurenic acid greater than cis 2,3 PDA greater than AP5. Moreover, only MK 801 was able to block the last population spike of the penicillin-induced epileptiform bursting in 100% of the experiments. The data indicate that the antiepileptic activity of E.A.A. antagonists on the penicillin epileptiform bursting in CA1 pyramidal cells is low and limited, indicating that the hippocampal area is not the primary site of the anticonvulsant activity of E.A.A. antagonists.
已经研究了兴奋性氨基酸（E.A.A.）拮抗剂如犬尿氨酸、2-氨基-5-磷酸戊酸（AP5）、顺式-2,3-哌啶二羧酸（顺式-2,3 PDA）和（+）-5-甲基-10,11-二氢-5H-二苯并（a,d）环庚烯-5,10-亚胺马来酸盐（MK 801）对浸浴在青霉素（1 mM）中的大鼠海马切片中诱发的癫痫样活动的抑制作用。抑制效力的顺序为：MK 801＞犬尿氨酸＞顺式2,3 PDA＞AP5。此外，在100%的实验中，只有MK 801能够阻断青霉素诱导的癫痫样爆发的最后一个群体峰电位。数据表明，E.A.A.拮抗剂对CA1锥体细胞中青霉素癫痫样爆发的抗癫痫活性较低且有限，这表明海马区不是E.A.A.拮抗剂抗惊厥活性的主要部位。
