Jang C G, Lee S Y
Department of Pharmacology, College of Pharmacy, Sungkyunkwan University, Suwon, Korea.
Arch Pharm Res. 2001 Dec;24(6):613-7. doi: 10.1007/BF02975175.
The present study examined the hypothesis that NMDA, AMPA/Kainate, and metabotropic (mGlu) glutamate receptors contribute to a behavioral stimulation induced by activation of dopamine receptors by comparing responses in apomorphine-induced cage climbing behaviors in mice. MK-801, CNQX, and MCPG were served as the NMDA receptor, AMPA/Kainate receptor, and mGlu receptor antagonist, respectively, to elucidate the glutamatergic modulation in apomorphine-induced dopaminergic activation in mice. Drugs were administered intracerebroventricularly (i.c.v.) into the mouse brain 15 min before the apomorphine treatment (2 mg/kg, s.c.). I.c.v. injection of MK-801 inhibited the apomorphine-induced cage climbing behavior dose-dependently. However, treatments with CNQX and MCPG did not any significant change in apomorphine-induced cage climbing behavior in mice. These results suggest that stimulation of NMDA type of glutamate receptors could contribute to the dopaminergic stimulation, but not AMPA/Kainate and mGlu type glutamate receptors.
本研究通过比较小鼠阿扑吗啡诱导的笼内攀爬行为的反应，检验了如下假说：N-甲基-D-天冬氨酸（NMDA）、α-氨基-3-羟基-5-甲基-4-异恶唑丙酸/海人藻酸（AMPA/海人藻酸）和代谢型（mGlu）谷氨酸受体参与了多巴胺受体激活所诱导的行为刺激。分别使用MK-801、CNQX和MCPG作为NMDA受体、AMPA/海人藻酸受体和mGlu受体拮抗剂，以阐明谷氨酸能对小鼠阿扑吗啡诱导的多巴胺能激活的调节作用。在阿扑吗啡处理（2mg/kg，皮下注射）前15分钟，将药物脑室内（i.c.v.）注射到小鼠脑内。脑室内注射MK-801剂量依赖性地抑制了阿扑吗啡诱导的笼内攀爬行为。然而，CNQX和MCPG处理并未使小鼠阿扑吗啡诱导的笼内攀爬行为发生任何显著变化。这些结果表明，谷氨酸受体的NMDA亚型的激活可能参与了多巴胺能刺激，但AMPA/海人藻酸和mGlu亚型谷氨酸受体并未参与。
