The cerebral cortex and parafascicular thalamic nucleus facilitate in vivo acetylcholine release in the rat striatum through distinct glutamate receptor subtypes
The cerebral cortex and parafascicular thalamic nucleus facilitate in vivo acetylcholine release in the rat striatum through distinct glutamate receptor subtypes
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DOI：
10.1111/j.1460-9568.1996.tb01565.x
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发表时间：
1996-12-01
影响因子：
3.4
通讯作者：
Nannini, L
中科院分区：
文献类型：
--
作者：
Consolo, S;Baldi, G;Nannini, L
经纹状体微透析证实，电刺激自由活动大鼠双侧额叶皮质或丘脑束旁核(10个脉冲0.5ms，10V，10a，频率10 Hz，电流140mA)可促进背侧纹状体乙酰胆碱的释放。易化效应可被5MU河豚毒素阻断，提示释放是神经元来源的。纹状体胆碱能神经元对前额叶皮质刺激的反应是短暂的，需要更长的刺激时间(20min)，而对丘脑刺激的反应(4min)才能达到最大效果。Alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic酸(AMPA)/海人酸谷氨酸能受体拮抗剂6，7-二硝基-2，3-二酮[DNQX；侧脑室注射(I.C.V.)，每侧12nmoL]和AMPA拮抗剂6-nitro-7-sulphamoylbenzo(f)quinoxaline-2，3-dione(NBQX；每侧12nmol，i.c.V.NMDA型受体拮抗剂MK-801(0.2 mg/kg，i.p.)可阻断刺激前额叶诱发的促进纹状体乙酰胆碱释放的作用。相反，DNQX或NBQX不能阻止刺激束旁核诱发的纹状体乙酰胆碱释放的增加，但MK-801与先前的结果一致。MK-801本身可降低纹状体乙酰胆碱的产量，而DNQX和NBQX则不能。结果表明，大脑皮层通过非紧张性激活AMPA型谷氨酸能受体促进背侧纹状体胆碱能活动，而束旁核通过紧张性激活NMDA受体促进背侧纹状体胆碱能活动。这两种谷氨酸受体可能都位于纹状体。总体结果表明，这两条通路通过不同的机制独立地调节纹状体胆碱能活动。
Electrical stimulation (ten pulses of 0.5 ms, 10 V applied over 10 a at 10 Hz, 140 mu A) delivered bilaterally to the prefrontal cortex or the parafascicular thalamic nucleus of freely moving rats facilitated acetylcholine release in dorsal striata, assessed by trans-striatal microdialysis. The facilitatory effects were blocked by coperfusion with 5 mu M tetrodotoxin, suggesting that the release was of neuronal origin. The response of the striatal cholinergic neurons to prefrontal cortical stimulation was short-lived and required a longer period of stimulation (20 min) than the response to thalamic stimulation (4 min) to reach maximal effect. The alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate glutamatergic receptor antagonist 6,7-dinitroquinoxaline-2,3-dione [DNQX; 12 nmol per side, intracerebroventricularly (i.c.v.)] and the AMPA antagonist 6-nitro-7-sulphamoylbenzo(f)quinoxaline-2,3-dione (NBQX; 12 nmol per side, i.c.v. or 12.8 mu M infused into the striatum), but not the NMDA-type receptor antagonist MK-801 (0.2 mg/kg, i.p.), abolished the facilitatory effect on striatal acetylcholine release evoked by stimulation of the prefrontal cortex. By contrast, DNQX or NBQX did not prevent the increase in striatal acetylcholine release evoked by parafascicular nucleus stimulation, but MK-801, in accordance with previous results, did so. MK-801 by itself lowered striatal acetylcholine output while DNQX and NBQX did not. The results provide in vivo evidence that the cerebral cortex facilitates cholinergic activity in the dorsal striatum apparently through the non-tonic activation of AMPA-type glutamatergic receptors while the parafascicular nucleus does this through tonic activation of NMDA receptors. Both glutamate receptor types are probably located in the striatum. The overall results suggest that the two pathways operate independently to regulate striatal cholinergic activity through distinct mechanisms.