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伏隔核中多巴胺的耗竭会阻止代谢型谷氨酸受体激活所引发的运动产生。

Depletion of dopamine in the nucleus accumbens prevents the generation of locomotion by metabotropic glutamate receptor activation.

作者信息

Meeker D, Kim J H, Vezina P

机构信息

Department of Psychiatry, The University of Chicago, 5841 S. Maryland Avenue, MC 3077, Chicago, IL 60637-1478, USA.

出版信息

Brain Res. 1998 Nov 23;812(1-2):260-4. doi: 10.1016/s0006-8993(98)00941-x.

DOI:10.1016/s0006-8993(98)00941-x
PMID:9813358
Abstract

The contribution of dopamine (DA) to the locomotion elicited by activation of nucleus accumbens (NAcc) metabotropic glutamate receptors (mGluRs) was investigated in the rat. Different groups of rats were pretreated with bilateral microinjections of either 6-hydroxydopamine (6-OHDA) or its vehicle into the NAcc and, on separate tests starting 10 days later, were tested for locomotion following microinjections (into the same site) of saline, the mGluR agonist, 1-aminocyclopentane-trans-1,3-dicarboxylic acid [(1S, 3R)-ACPD, 0.5 nmol/side] and amphetamine (AMPH, 6.8 nmol/side). DA levels at the microinjection sites were significantly depleted in 6-OHDA-treated rats (42-99% depletions compared to control values obtained in vehicle-treated rats). In contrast to the increased locomotion observed in non-lesioned animals, rats pretreated with 6-OHDA showed no increase in locomotor activity in response to (1S, 3R)-ACPD or AMPH when these were microinjected into the NAcc. The two groups of rats were indistinguishable when tested following NAcc saline. These findings suggest that, as with AMPH, enhanced locomotion produced by NAcc mGluR activation is dependent on intact DA neurotransmission in this site.

摘要

在大鼠中研究了多巴胺(DA)对伏隔核(NAcc)代谢型谷氨酸受体(mGluRs)激活所引发运动的作用。将不同组的大鼠双侧微量注射6-羟基多巴胺(6-OHDA)或其溶媒预处理至NAcc,在10天后开始的单独测试中,在微量注射(至相同部位)生理盐水、mGluR激动剂1-氨基环戊烷-反式-1,3-二羧酸[(1S,3R)-ACPD,0.5 nmol/侧]和苯丙胺(AMPH,6.8 nmol/侧)后测试其运动情况。在6-OHDA处理的大鼠中,微量注射部位的DA水平显著降低(与溶媒处理大鼠获得的对照值相比,降低了42-99%)。与未损伤动物中观察到的运动增加相反,用6-OHDA预处理的大鼠在将(1S,3R)-ACPD或AMPH微量注射至NAcc时,运动活性没有增加。当在NAcc注射生理盐水后进行测试时,两组大鼠没有差异。这些发现表明,与AMPH一样,NAcc mGluR激活产生的运动增强依赖于该部位完整的DA神经传递。

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Depletion of dopamine in the nucleus accumbens prevents the generation of locomotion by metabotropic glutamate receptor activation.伏隔核中多巴胺的耗竭会阻止代谢型谷氨酸受体激活所引发的运动产生。
Brain Res. 1998 Nov 23;812(1-2):260-4. doi: 10.1016/s0006-8993(98)00941-x.
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