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首页> 外文期刊>The European Journal of Neuroscience >Lesion of medial prefrontal dopamine terminals abolishes habituation of accumbens shell dopamine responsiveness to taste stimuli
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Lesion of medial prefrontal dopamine terminals abolishes habituation of accumbens shell dopamine responsiveness to taste stimuli

机译：前额内侧多巴胺末端的病变消除了伏隔壳多巴胺对味觉刺激的适应性

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摘要

Taste stimuli increase extracellular dopamine (DA) in the nucleus accumbens (NAc) and in the medial prefrontal cortex (mPFC). This effect shows single-trial habituation in NAc shell but not in core or in mPFC. Morphine sensitization abolishes habituation of DA responsiveness in NAc shell but induces it in mPFC. These observations support the hypothesis of an inhibitory influence of mPFC DA on NAc DA. To test this hypothesis, we used in vivo microdialysis to investigate the effect of mPFC 6-hydroxy-dopamine (6-OHDA) lesions on the NAc DA responsiveness to taste stimuli. 6-OHDA was infused bilaterally in the mPFC of rats implanted with guide cannulae. After 1 week, rats were implanted with an intraoral catheter, microdialysis probes were inserted into the guide cannulae, and dialysate DA was monitored in NAc shell/core after intraoral chocolate. 6-OHDA infusion reduced tissue DA in the mPFC by 75%. Tyrosine hydroxylase immunohistochemistry showed that lesions were confined to the mPFC. mPFC 6-OHDA lesion did not affect the NAc shell DA responsiveness to chocolate in naive rats but abolished habituation in rats pre-exposed to the taste. In the NAc core, mPFC lesion potentiated, delayed and prolonged the stimulatory DA response to taste but failed to affect DA in pre-exposed rats. Behavioural taste reactions and motor activity were not affected. The results indicate a top-down control of NAc DA by mPFC and a reciprocal relationship between DA transmission in these two areas. Moreover, habituation of DA responsiveness in the NAc shell is dependent upon an intact DA input to the mPFC. ? 2012 Federation of European Neuroscience Societies and Blackwell Publishing Ltd.
机译：味觉刺激增加伏伏核（NAc）和前额内侧皮层（mPFC）中的细胞外多巴胺（DA）。此效果显示在NAc外壳中单次尝试适应，但在核心或mPFC中则没有。吗啡敏化消除了NAc外壳中DA反应的习惯，但在mPFC中诱导了它。这些观察结果支持了mPFC DA对NAc DA的抑制作用的假说。为了验证该假设，我们使用体内微透析技术研究了mPFC 6-羟基-多巴胺（6-OHDA）损伤对NAc DA对味觉刺激的反应性的影响。将6-OHDA双向注入植入引导套管的大鼠的mPFC中。 1周后，将大鼠植入口内导管，将微透析探针插入引导套管中，并在口内巧克力后在NAc壳/核中监测透析液DA。 6-OHDA输注可使mPFC中的组织DA降低75％。酪氨酸羟化酶免疫组化显示病变仅限于mPFC。 mPFC 6 -OHDA损伤不影响幼稚大鼠的NAc壳DA对巧克力的反应性，但消除了预先暴露于味觉的大鼠的习惯性。在NAc核心，mPFC病变增强，延迟和延长了DA对味觉的刺激反应，但未影响预暴露大鼠的DA。行为味觉反应和运动活动不受影响。结果表明，通过mPFC对NAc DA进行了自上而下的控制，这两个区域的DA传输之间存在相互关系。此外，NAc外壳中DA响应能力的习惯取决于输入到mPFC的完整DA。 ？ 2012年欧洲神经科学学会联合会和布莱克韦尔出版有限公司。

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