• M Jabourian, S Bourgoin, S Pérez, G Godeheu, J Glowinski, and M-L Kemel.
• INSERM U114, Collège de France, 11 place Marcelin Berthelot, 75231, Cedex 05, Paris, France. maritza.jabourian@college.de-france.fr
• Neuroscience. 2004 Jan 1; 123 (3): 733-42.

AbstractUsing 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.

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