Li R, Wing L L, Kirch D G, Wyatt R J, Chuang D M
Neuropsychiatry Branch, National Institute of Mental Health, Neuroscience Center at Saint Elizabeths, Washington, DC 20032.
Psychopharmacology (Berl). 1992;109(1-2):248-50. doi: 10.1007/BF02245510.
Muscarinic receptor-mediated phosphoinositide (PI) turnover in rat brain slices was assessed after chronic administration of nicotine (12 mg/kg/day) or haloperidol decanoate (1.5 mg/kg/day), either alone or in combination, for 6 weeks. Nicotine alone did not significantly alter carbachol-induced inositol monophosphate (IP1) accumulation in the frontal cortex, but did result in a significant increase in the hippocampus, and in a decrease in the striatum. Haloperidol alone attenuated carbachol-stimulated IP1 accumulation in all three brain regions. Chronic treatment with combined nicotine and haloperidol resulted in no significant change in carbachol-sensitive IP1 accumulation in either the frontal cortex or hippocampus but did result in a decrease in the striatum. The results suggest significant cross-talk between cholinergic and dopaminergic systems in affecting PI metabolism.
在大鼠脑片中，评估了慢性给予尼古丁（12毫克/千克/天）或癸酸氟哌啶醇（1.5毫克/千克/天）单独或联合使用6周后毒蕈碱受体介导的磷酸肌醇（PI）转换情况。单独使用尼古丁并未显著改变卡巴胆碱诱导的额叶皮质中肌醇单磷酸（IP1）的积累，但确实导致海马体中IP1显著增加，而纹状体中则减少。单独使用氟哌啶醇减弱了卡巴胆碱刺激的所有三个脑区中IP1的积累。尼古丁和氟哌啶醇联合慢性治疗导致额叶皮质或海马体中对卡巴胆碱敏感的IP1积累无显著变化，但确实导致纹状体中减少。结果表明胆碱能和多巴胺能系统在影响PI代谢方面存在显著的相互作用。
