Tarnawa I, Molnár P, Gaál L, Andrási F
Institute for Drug Research, Budapest, Hungary.
Acta Physiol Hung. 1992;79(2):163-9.
GYKI 52466 is a specific antagonist of the neuronal excitation mediated by the non-NMDA type excitatory amino acid receptors, at several sites in the central nervous system. The experiments presented here show that the drug has a dose-dependent, slowly developing, long-lasting and reversible inhibitory action on the field potentials recorded from the CA1 region of the rat hippocampus, in vitro. Its action is similar to that of the well-known non-NMDA receptor blocker, CNQX. When the stimulus intensity-dependence of the population spikes was investigated, both drugs shifted the input-output curves in a parallel manner, while the maximum responses were only slightly depressed at the doses applied. With i.v. application, GYKI 52466 also inhibited the hippocampal field potentials recorded from the CA1 region of anesthetized rats dose-dependently. The inhibition was relatively weak compared to the effect found in earlier studies in the spinal cord, by the same doses. Four mg/kg i.v., a doses which is able to block spinal reflexes completely, caused an only about 20% depression of the recorded responses in the hippocampal CA1 area.
GYKI 52466是一种非NMDA型兴奋性氨基酸受体介导的神经元兴奋的特异性拮抗剂,作用于中枢神经系统的多个部位。本文所呈现的实验表明,该药物对体外记录的大鼠海马CA1区场电位具有剂量依赖性、缓慢发展、持久且可逆的抑制作用。其作用类似于著名的非NMDA受体阻滞剂CNQX。当研究群体峰电位的刺激强度依赖性时,两种药物均以平行方式使输入-输出曲线发生位移,而在所应用的剂量下,最大反应仅略有降低。静脉注射时,GYKI 52466也剂量依赖性地抑制麻醉大鼠海马CA1区记录的场电位。与早期在脊髓研究中相同剂量所产生的效应相比,该抑制作用相对较弱。静脉注射4mg/kg,这一能够完全阻断脊髓反射的剂量,仅使海马CA1区记录的反应降低约20%。