title: Mu opioid control of the N-methyl-D-aspartate-evoked release of [3H]-acetylcholine in the limbic territory of the rat striatum in vitro: diurnal variations and implication of a dopamine link.
abstract: 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.
authors.affiliation: INSERM U114, Collège de France, 11 place Marcelin Berthelot, 75231, Cedex 05, Paris, France. maritza.jabourian@college.de-france.fr
authors.forename: M
authors.initials: M
authors.lastname: Jabourian
authors.forename: S
authors.initials: S
authors.lastname: Bourgoin
authors.forename: S
authors.initials: S
authors.lastname: Pérez
authors.forename: G
authors.initials: G
authors.lastname: Godeheu
authors.forename: J
authors.initials: J
authors.lastname: Glowinski
authors.forename: M-L
authors.initials: ML
authors.lastname: Kemel
mesh_terms: D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D002940:Circadian Rhythm / Q000187:drug effects / Q000502:physiology*; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism*; D004298:Dopamine / Q000378:metabolism; D008032:Limbic System / Q000187:drug effects / Q000378:metabolism; D008297:Male; D009271:Naltrexone / Q000031:analogs & derivatives* / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000819:agonists / Q000378:metabolism*; D017450:Receptors, Opioid, mu / Q000037:antagonists & inhibitors / Q000378:metabolism*; D014316:Tritium
chemical_list: D016194:Receptors, N-Methyl-D-Aspartate; D017450:Receptors, Opioid, mu; D014316:Tritium; D009271:Naltrexone; C024524:beta-funaltrexamine; D000109:Acetylcholine; D004298:Dopamine