Hanson G R, Singh N, Merchant K, Johnson M, Gibb J W
Department of Pharmacology and Toxicology, University of Utah, Salt Lake City 84112, USA.
Drug Alcohol Depend. 1995 Feb;37(2):107-10. doi: 10.1016/0376-8716(94)01065-s.
High doses of stimulants of abuse, such as methamphetamine and cocaine, cause significant increases in the content of neurotension- and dynorphin-like immunoreactivity in the striatum and nucleus accumbens (approximately 200-600% of control) in the rat. These changes in neuropeptide content are caused by stimulation of dopamine D1 receptors and prevented by the glutamate NMDA receptor antagonist, MK 801. Stimulation of the NMDA receptor with N-methyl-D-aspartate results in increases in the neuropeptide levels like that caused by methamphetamine and cocaine. These findings demonstrate that stimulants of abuse profoundly influence neurotensin and dynorphin pathways associated with extrapyramidal and limbic structures by an interaction of activated dopamine D1 and glutamate NMDA receptors.
高剂量的滥用兴奋剂，如甲基苯丙胺和可卡因，会使大鼠纹状体和伏隔核中神经降压素和强啡肽样免疫反应性的含量显著增加（约为对照组的200%-600%）。这些神经肽含量的变化是由多巴胺D1受体的刺激引起的，并可被谷氨酸N-甲基-D-天冬氨酸（NMDA）受体拮抗剂MK 801阻断。用N-甲基-D-天冬氨酸刺激NMDA受体可导致神经肽水平升高，类似于甲基苯丙胺和可卡因所引起的情况。这些发现表明，滥用兴奋剂通过激活的多巴胺D1受体和谷氨酸NMDA受体之间的相互作用，深刻影响与锥体外系和边缘结构相关的神经降压素和强啡肽途径。
