Hara S, Mukai T, Kuriiwa F, Iwata N, Yanase T, Kano S, Endo T
Department of Forensic Medicine, Tokyo Medical College, Japan.
Life Sci. 1997;61(20):PL 289-94. doi: 10.1016/s0024-3205(97)00867-9.
Intracerebroventricular (i.c.v.) administration of N-methyl-D-aspartate (NMDA) caused a biphasic rise of brain temperature, namely, a rapid, early rise and a larger, late rise, in urethane-anesthetized rats. I.c.v. pretreatment with a noncompetitive NMDA receptor antagonist, MK-801, attenuated the late rise of the brain temperature, but had no effect on the early rise, whereas i.c.v. pretreatment with a competitive NMDA receptor antagonist, (+/-)-2-amino-5-phosphonopentanoic acid (AP-5), attenuated both rises. AP-5 per se caused a rise in brain temperature without any rise of rectal temperature, whereas MK-801 per se caused no significant change of the brain or rectal temperature. This rise by AP-5 was suppressed by MK-801, suggesting an agonistic effect of AP-5 on NMDA receptors in rat brain in vivo.
在氨基甲酸乙酯麻醉的大鼠中，脑室内（i.c.v.）注射N-甲基-D-天冬氨酸（NMDA）会引起脑温双相升高，即快速的早期升高和幅度更大的晚期升高。用非竞争性NMDA受体拮抗剂MK-801进行脑室内预处理可减弱脑温的晚期升高，但对早期升高无影响，而用竞争性NMDA受体拮抗剂（±）-2-氨基-5-磷酸戊酸（AP-5）进行脑室内预处理则可减弱这两种升高。AP-5本身会引起脑温升高而直肠温度无升高，而MK-801本身对脑温和直肠温度均无显著影响。AP-5引起的这种升高被MK-801抑制，提示AP-5在体内对大鼠脑内NMDA受体具有激动作用。
