ROLE OF DYNORPHIN-CONTAINING NEURONS IN THE PRESYNAPTIC INHIBITORY CONTROL OF THE ACETYLCHOLINE-EVOKED RELEASE OF DOPAMINE IN THE STRIOSOMES AND THE MATRIX OF THE CAT CAUDATE-NUCLEUS
ROLE OF DYNORPHIN-CONTAINING NEURONS IN THE PRESYNAPTIC INHIBITORY CONTROL OF THE ACETYLCHOLINE-EVOKED RELEASE OF DOPAMINE IN THE STRIOSOMES AND THE MATRIX OF THE CAT CAUDATE-NUCLEUS
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DOI：
10.1016/0306-4522(91)90340-t
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发表时间：
1991-01-01
期刊：
影响因子：
3.3
通讯作者：
KEMEL, ML
中科院分区：
文献类型：
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作者：
GAUCHY, C;DESBAN, M;KEMEL, ML
在猫尾状核的一个显著的纹状体富集区和一个邻近的基质富集区，研究了乙酰胆碱和强啡肽（1-13）在突触前控制由[H-3]酪氨酸连续合成的[H-3]多巴胺释放中的作用。这是通过将微灌注装置垂直应用于猫脑冠状切片来实现的。这些装置被放置在位于结构核心的纹状体富集区（乙酰胆碱酯酶贫乏区）和相邻的基质富集区（乙酰胆碱酯酶富集区）。将[H-3]酪氨酸连续输送至每个微灌注装置，并估计灌注液中释放的[H-3]多巴胺。如前所示，在河豚毒素（1 μ M）的存在下，乙酰胆碱（50 μ M）通过与毒蕈碱受体的相互作用诱导两个隔室中[H-3]多巴胺释放的延长刺激。我们目前的研究表明，强啡肽1-13（1 μ M）和选择性κ激动剂反式-3，4-二氯-N-甲基-N-[2-（1-吡咯烷基）环己基]苯乙酰胺（U 50488）（1 μ M）抑制河豚毒素抗性乙酰胆碱诱发的[H-3]多巴胺释放，这些作用在基质中比在纹状体富集区稍微更明显。纳洛酮（1 μ M）逆转U 50488在这两个领域的抑制作用。这些结果表明，强啡肽通过位于纹状体和基质中多巴胺神经末梢上的κ阿片受体对多巴胺释放进行抑制性突触前控制，然而，在基质中多巴胺释放的突触前胆碱能控制比在纹状体富集区复杂得多。除了河豚毒素抵抗的刺激作用外，乙酰胆碱对[H-3]多巴胺的释放产生两种相反的河豚毒素敏感的作用，一种是易化的，另一种是抑制的。我们在这里证明，在灌流的基质富集区，间接的乙酰胆碱抑制反应是由含强啡肽的神经元介导的。事实上，乙酰胆碱对[H-3]多巴胺释放的短暂刺激作用在纳洛酮（1 μ M）的存在下转化为持久的反应，在后一种情况下，强啡肽1-13（1 μ M）的共同应用恢复了短暂的刺激作用。
The roles of acetylcholine and dynorphin (1-13) in the presynaptic control of the release of [H-3]dopamine continuously synthesized from [H-3]tyrosine were examined in a prominent striosomal enriched area and in an adjacent matrix enriched area of the cat caudate nucleus. This was achieved using microsuperfusion devices applied vertically onto coronal slices of cat brain. These devices were placed in a striosomal enriched area located in the core of the structure (acetylcholinesterase-poor zone) and in an adjacent matrix enriched area (acetylcholinesterase-rich zone). [H-3]Tyrosine was delivered continuously to each microsuperfusion device and [H-3]dopamine released was estimated in the superfusate. As previously shown, in the presence of tetrodotoxin (1-mu-M), acetylcholine (50-mu-M) induces a prolonged stimulation of [H-3]dopamine release in both compartments through an interaction with muscarinic receptors. Our present study indicates that both dynorphin 1-13 (1-mu-M) and the selective kappa agonist trans-3,4-dichloro-N-methyl-N [2-(1-pyrrolidinyl)cyclohexyl]benzenacetamine (U50488) (1-mu-M) inhibit the tetrodotoxin-resistant acetylcholine-evoked release of [H-3]dopamine, these effects being slightly more pronounced in the matrix than in the striosomal enriched area. Naloxone (1-mu-M) reversed the inhibitory effect of U50488 in both areas. These results suggest that dynorphin exerts an inhibitory presynaptic control of dopamine release through kappa opioid receptors located on dopamine nerve terminals in the striosome as well as in the matrix.However, the presynaptic cholinergic control of dopamine release is much more complex in the matrix than in the striosomal enriched area. Besides its tetrodotoxin-resistant stimulatory effect, acetylcholine exerts two opposing tetrodotoxin-sensitive effects on [H-3]dopamine release, one facilitatory and the other inhibitory.We demonstrate here that in the superfused matrix enriched area, the indirect acetylcholine inhibitory response is mediated by dynorphin-containing neurons. Indeed, the short-lasting stimulatory effect of acetylcholine on [H-3]dopamine release was converted into a long-lasting response in the presence of naloxone (1-mu-M), and, in this latter condition, the co-application of dynorphin 1-13 (1-mu-M) restored the short-lasting stimulatory effect.