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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Neurochemical evidence that stimulation of CB1 cannabinoid receptors on GABAergic nerve terminals activates the dopaminergic reward system by increasing dopamine release in the rat nucleus accumbens.
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Neurochemical evidence that stimulation of CB1 cannabinoid receptors on GABAergic nerve terminals activates the dopaminergic reward system by increasing dopamine release in the rat nucleus accumbens.

机译：神经化学证据表明，通过刺激大鼠伏隔核中多巴胺的释放，刺激GABA能神经末梢上的CB1大麻素受体激活多巴胺能奖励系统。

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摘要

We examined the effect of cannabinoid receptor activation on basal and electrical field simulation-evoked (25 V, 2 Hz, 240 shocks) [(3)H]dopamine efflux in the isolated rat nucleus accumbens in a preparation, in which any effect on the dendrites or somata of ventral tegmental projection neurons was excluded. The cannabinoid agonist (R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)pyrrolo[1,2,3-de]-1,4-benzox azin-6-yl]-1-naphthalenylmethanone mesylate (WIN55,212-2, 100 nM) significantly enhanced stimulation-evoked [(3)H]dopamine release in the presence of the selective dopamine transporter inhibitor 1-[2-[bis-(4-fluorophenyl)methoxy]ethyl]-4-(3-phenylpropyl)piperazine dihydrochloride (GBR12909, 100 nM). GBR12909 (100 nM-1 microM), when added alone, increased the evoked [(3)H]dopamine efflux in a concentration-dependent manner. The stimulatory effect of WIN55,212-2 on the evoked tritium efflux was inhibited by the selective CB1 cannabinoid receptor antagonist N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3 -carboxamide (AM251, 100 nM) and by the GABA(A) receptor antagonist bicuculline (10 microM). Repeated application of N-methyl-d aspartate (1 mM) under Mg(2+)-free conditions, which directly acts on dopaminergic terminals, reversibly increased the tritium efflux, but WIN55,212-2 did not affect N-methyl-d aspartate-evoked [(3)H]dopamine efflux, indicating that WIN55,212-2 has no direct action on dopaminergic nerve terminals. AM251 (100 nM) alone also did not have an effect on electrical stimulation-evoked [(3)H]dopamine efflux. Likewise, the selective CB2 receptor antagonist 6-iodo-2-methyl-1-[2-(4-morpholinyl)ethyl]-1H-indol-3-yl](4-methoxyphenyl)methano ne (AM630, 0.3 microM) and the anandamide transport inhibitor (5Z,8Z,11Z,14Z)-N-(4-hydroxy-2-methylphenyl)-5,8,11,14-eicosatetraenamide (VDM11, 10 microM) had no significant effect on electrically evoked [(3)H]dopamine release. This is the first neurochemical evidence that the activation of CB1 cannabinoid receptors leads to the augmentation of [(3)H]dopamine efflux via a local GABA(A) receptor-mediated disinhibitory mechanism in the rat nucleus accumbens.
机译：我们检查了大麻素受体激活对基础和电场模拟诱发的（25 V，2 Hz，240次电击）[（3）H]多巴胺流出在制备的分离的大鼠伏隔核中的作用，其中对排除腹侧被盖投射神经元的树突或躯体。大麻素激动剂（R）-（+）-[2,3-二氢-5-甲基-3-（4-吗啉基甲基）吡咯并[1,2,3-de] -1,4-苯并a嗪-6-基在选择性多巴胺转运蛋白抑制剂1- [2- [双-（4-氟苯基）存在下]]-1-萘甲磺酸甲磺酸萘酯（WIN55,212-2，100 nM）显着增强了刺激诱发的[（3）H]多巴胺释放）（甲氧基]乙基] -4-（3-苯基丙基）哌嗪二盐酸盐（GBR12909，100 nM）。当单独添加GBR12909（100 nM-1 microM）时，以浓度依赖的方式增加了诱发的[（3）H]多巴胺流出。选择性CB1大麻素受体拮抗剂N-（哌啶-1-基）-5-（4-碘苯基）-1-（2,4-二氯苯基）抑制了WIN55,212-2对诱发的tri外流的刺激作用。 -4-甲基-1H-吡唑-3-羧酰胺（AM251，100 nM）和由GABA（A）受体拮抗剂bicuculline（10 microM）组成。在无Mg（2+）的条件下重复应用N-甲基-d天冬氨酸（1 mM），直接作用于多巴胺能末端，可逆地增加了的外排量，但WIN55,212-2并不影响N-甲基-d天冬氨酸引起的[（3）H]多巴胺流出，表明WIN55,212-2对多巴胺能神经末梢没有直接作用。单独的AM251（100 nM）也对电刺激诱发的[（3）H]多巴胺流出没有影响。同样，选择性CB2受体拮抗剂6-碘-2-甲基-1- [2-（4-吗啉基）乙基] -1H-吲哚-3-基]（4-甲氧基苯基）亚甲基（AM630，0.3 microM）和Anandamide转运抑制剂（5Z，8Z，11Z，14Z）-N-（4-羟基-2-甲基苯基）-5,8,11,14-二十碳四烯酰胺（VDM11，10 microM）对电诱发的脑电无明显影响[[（ 3）H]多巴胺释放。这是第一个神经化学证据，表明CB1大麻素受体的激活通过大鼠伏伏核中的局部GABA（A）受体介导的去抑制机制导致[（3）H]多巴胺外排的增加。

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