Kayadjanian N, Rétaux S, Menétrey A, Besson M J
Laboratoire de Neurochimie-Anatomie, CNRS URA 1488, Institut des Neurosciences, Université Pierre et Marie Curie, Paris, France.
Brain Res. 1994 Jun 27;649(1-2):129-35. doi: 10.1016/0006-8993(94)91056-1.
The effect of (-)-nicotine on the spontaneous release of [3H]gamma-aminobutyric acid ([3H]GABA) was studied in vitro in rat substantia nigra (SN) and globus pallidus (GP) slices. In both structures, nicotine (10(-4) M) elicited a transient increase of [3H]GABA release lasting no more than 2.5 min. At the peak of the effect, a 18.5% and 25% increase of [3H]GABA was observed in GP and SN slices, respectively. At lower concentration (10(-5) M), nicotine produced a small but significant transient increase (+8%) in GP slices whereas this concentration was ineffective in SN slices. Pempidine (10(-5) M) totally antagonized the 10(-4) M nicotine-induced effect in SN and GP. The increase of [3H]GABA release elicited by 10(-4) M nicotine was abolished when Ca2+ concentration in the superfusion medium was lowered from 2.4 to 0.4 mM. To investigate a possible dopaminergic (DA) link in the response, we examined the sensitivity of the nicotine-induced effect to DA D1 (SCH23390) and D2 (sulpiride) receptor antagonists. In SN, SCH23390 (10(-6) M) abolished the 10(-4) M nicotine-induced effect. In GP, sulpiride (10(-5) M) failed to modify the response. Moreover, SCH23390 partially reversed the nicotine-induced effect (-37%) in GP. Taken together these results indicate that nicotine differentially modulate the [3H]GABA release in SN and GP. In SN, the nicotine-induced [3H]GABA release appears to be mediated by DA neurons. In GP, only a part of the nicotinic response involved a DA link. A possible direct stimulation of nicotinic receptors localized on striato-pallidal terminals is discussed.
在大鼠黑质（SN）和苍白球（GP）脑片上，对（-）-尼古丁对[3H]γ-氨基丁酸（[3H]GABA）自发释放的影响进行了体外研究。在这两种结构中，尼古丁（10^-4 M）引起[3H]GABA释放短暂增加，持续时间不超过2.5分钟。在效应峰值时，在GP和SN脑片中分别观察到[3H]GABA增加了18.5%和25%。在较低浓度（10^-5 M）时，尼古丁在GP脑片中产生了小但显著的短暂增加（+8%），而该浓度在SN脑片中无效。潘必啶（10^-5 M）完全拮抗了10^-4 M尼古丁在SN和GP中诱导的效应。当灌流液中Ca2+浓度从2.4 mM降至0.4 mM时，10^-4 M尼古丁引起的[3H]GABA释放增加被消除。为了研究反应中可能的多巴胺能（DA）联系，我们检测了尼古丁诱导的效应对DA D1（SCH23390）和D2（舒必利）受体拮抗剂的敏感性。在SN中，SCH23390（10^-6 M）消除了10^-4 M尼古丁诱导的效应。在GP中，舒必利（10^-5 M）未能改变反应。此外，SCH23390部分逆转了GP中尼古丁诱导的效应（-37%）。综上所述，这些结果表明尼古丁对SN和GP中[3H]GABA的释放有不同的调节作用。在SN中，尼古丁诱导的[3H]GABA释放似乎由DA神经元介导。在GP中，只有部分烟碱反应涉及DA联系。文中讨论了对位于纹状体-苍白球终末的烟碱受体可能的直接刺激作用。
