Role of the parafascicular thalamic nucleus and N-methyl-D-aspartate transmission in the D-1-dependent control of in vivo acetylcholine release in rat striatum
Role of the parafascicular thalamic nucleus and N-methyl-D-aspartate transmission in the D-1-dependent control of in vivo acetylcholine release in rat striatum
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DOI：
10.1016/0306-4522(95)00421-1
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发表时间：
1996-03-01
期刊：
影响因子：
3.3
通讯作者：
DiChiara, G
中科院分区：
文献类型：
--
作者：
Consolo, S;Baronio, P;DiChiara, G
我们研究了参与的D-1受体介导的刺激乙酰胆碱流出在背侧纹状体在自由活动的大鼠，和丘脑纹状体和皮质纹状体通路在这种调节中的相对作用，在体内微透析的调制amatergic神经传递。选择性N-甲基-D-天冬氨酸非竞争性拮抗剂马来酸地佐环平（0.1 mg/kg i. p.），而不是红藻氨酸/使君子酸受体拮抗剂，6，7-二硝基喹喔啉-2，3-二酮（每侧i. c. v. 3 μ g），完全阻止由最大有效剂量的完全D-1激动剂SKF 82958（3 mg/kg s.c.）和多巴胺受体激动剂d-安非他明（2 mg/kg s.c.）。丘脑束旁核的急性双侧电解损伤阻止了SKF 82958和d-苯丙胺对纹状体乙酰胆碱输出的刺激，但仅轻微降低了基础乙酰胆碱的释放。相反，皮质纹状体通路的急性中断并没有改变这两种多巴胺能药物的作用，虽然它显着减少基础纹状体乙酰胆碱的释放。丘脑束旁核病变，或低剂量马来酸地佐环平（0.1 mg/kg i. p.），也阻止了神经安定剂Remoxipride（10 mg/kg s.c.）的乙酰胆碱增加作用，已知该效应是D-1受体依赖性的。结果表明，来自丘脑束旁核并利用N-甲基-D-天冬氨酸受体的纹状体投射在D-1介导的刺激背侧纹中乙酰胆碱释放中发挥关键作用。
We investigated the involvement of glutamatergic neurotransmission in the modulation of D-1 receptor-mediated stimulation of acetylcholine outflow in dorsal striatum in freely moving rats, and the relative roles of the thalamostriatal and corticostriatal pathways in this regulation using in vivo microdialysis. The selective n-methyl-D-aspartate non-competitive antagonist dizocilpine maleate (0.1 mg/kg i.p.), but not the kainate/quisqualate receptor antagonist, 6,7-dinitroquinoxaline-2,3-dione (3 mu g per side i.c.v.), completely prevented the rise in striatal extracellular acetylcholine elicited by maximal effective doses of the full D-1 agonist SKF 82958 (3 mg/kg s.c.) and of the dopamine releaser d-amphetamine (2 mg/kg s.c.). Acute bilateral electrolytic lesions of the parafascicular nucleus of the thalamus prevented the stimulation of striatal acetylcholine output by SKF 82958 and d-amphetamine but only slightly reduced basal acetylcholine release. In contrast acute interruption of the corticostriatal pathway did not alter the effect of the two dopaminergic drugs although it markedly reduced basal striatal acetylcholine release. Lesions of the parafascicular thalamic nucleus, or a low dose of dizocilpine maleate (0.1 mg/kg i.p.), also prevented the acetylcholine-increasing effect of the neuroleptic remoxipride (10 mg/kg s.c.), an effect known to be D-1 receptor dependent.The results suggest that striatal projections arising from the parafascicular thalamic nucleus and utilizing N-methyl-D-aspartate receptors play a critical role in the D-1-mediated stimulation of acetylcholine release in dorsal striata.