Jabourian M, Bourgoin S, Pérez S, Godeheu G, Glowinski J, Kemel M-L
INSERM U114, Collège de France, 11 place Marcelin Berthelot, 75231, Cedex 05, Paris, France.
Neuroscience. 2004;123(3):733-42. doi: 10.1016/j.neuroscience.2003.10.017.
Using an in vitro microsuperfusion procedure, the release of newly synthesized [(3)H]-acetylcholine (ACh), evoked by N-methyl-D-aspartate (NMDA) receptor stimulation, was investigated in striosome-enriched areas and matrix of the rat striatum. The role of micro-opioid receptors, activated by endogenously released enkephalin, on the NMDA-evoked release of ACh was studied using the selective micro-opioid receptor antagonist, beta-funaltrexamine. Experiments were performed 2 (morning) or 8 (afternoon) h after light onset, in either the presence or absence (alpha-methyl-p-tyrosine, an inhibitor of dopamine synthesis) of dopaminergic transmission. As expected, based on the presence of micro-opioid receptors in striosomes, beta-funaltrexamine (0.1 nM, 10 nM and 1 microM) enhanced the NMDA (1 mM+10 microM D-serine)-evoked release of ACh in striosome-enriched areas but not in the matrix. Interestingly, these responses were significantly more pronounced in afternoon than in morning experiments. In the presence of alpha-methyl-p-tyrosine, the NMDA-evoked release of ACh was increased with similar amplitude in morning and afternoon experiments. However, in this condition (without dopamine transmission), the facilitatory effects of beta-funaltrexamine on the NMDA-evoked release of ACh were suppressed totally in the morning and only partially in the afternoon. The selective micro-opiate agonist, [D-Ala(2),N-Me-Phe(4),Gly(5)-ol]-enkephalin (1 microM, coapplied with NMDA), was without effect on the NMDA-evoked release of ACh but abolished both dopamine-dependent (morning) and dopamine-independent (afternoon) responses of beta-funaltrexamine (10 nM and 1 microM).Therefore, in the limbic territory of the striatum enriched in striosomes, the micro-opioid-inhibitory regulation of ACh release follows diurnal rhythms. While dopamine is required for this regulation in the morning and the afternoon, an additional dopamine-independent process is present only in the afternoon.
采用体外微灌流程序，研究了在大鼠纹状体富含纹状体小体的区域和基质中，N - 甲基 - D - 天冬氨酸（NMDA）受体刺激诱发的新合成的[³H] - 乙酰胆碱（ACh）的释放。使用选择性微阿片受体拮抗剂β - 芬太尼环唑，研究了内源性释放的脑啡肽激活的微阿片受体对NMDA诱发的ACh释放的作用。实验在光照开始后2小时（上午）或8小时（下午）进行，分别在存在或不存在多巴胺能传递（α - 甲基 - p - 酪氨酸，一种多巴胺合成抑制剂）的情况下进行。正如预期的那样，基于纹状体小体中存在微阿片受体，β - 芬太尼环唑（0.1 nM、10 nM和1 μM）增强了富含纹状体小体区域中NMDA（1 mM + 10 μM D - 丝氨酸）诱发的ACh释放，但在基质中没有增强。有趣的是，这些反应在下午的实验中比上午的实验中明显更显著。在存在α - 甲基 - p - 酪氨酸的情况下，上午和下午实验中NMDA诱发的ACh释放以相似的幅度增加。然而，在这种情况下（没有多巴胺传递），β - 芬太尼环唑对NMDA诱发的ACh释放的促进作用在上午完全被抑制，而在下午仅部分被抑制。选择性微阿片激动剂[D - Ala(2)，N - Me - Phe(4)，Gly(5) - ol] - 脑啡肽（1 μM，与NMDA共同应用）对NMDA诱发的ACh释放没有影响，但消除了β - 芬太尼环唑（10 nM和1 μM）的多巴胺依赖性（上午）和多巴胺非依赖性（下午）反应。因此，在富含纹状体小体的纹状体边缘区域，ACh释放的微阿片抑制调节遵循昼夜节律。虽然上午和下午这种调节都需要多巴胺，但仅在下午存在一个额外的多巴胺非依赖性过程。
