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多巴胺能对食欲性痕迹条件反射的调节:内侧前额叶皮质中D1受体的作用

Dopaminergic modulation of appetitive trace conditioning: the role of D1 receptors in medial prefrontal cortex.

作者信息

Pezze M A, Marshall H J, Cassaday H J

机构信息

School of Psychology, University of Nottingham, University Park, Nottingham, NG7 2RD, UK.

出版信息

Psychopharmacology (Berl). 2015 Aug;232(15):2669-80. doi: 10.1007/s00213-015-3903-4. Epub 2015 Mar 29.

Abstract

RATIONALE

Trace conditioning may provide a behavioural model suitable to examine the maintenance of 'on line' information and its underlying neural substrates.

OBJECTIVES

Experiment la was run to establish trace conditioning in a shortened procedure which would be suitable to test the effects of dopamine (DA) D1 receptor agents administered by microinjection directly into the brain. Experiment lb examined the effects of the DA D1 agonist SKF81297 and the DA D1 antagonist SCH23390 following systemic administration in pre-trained animals. Experiment 2 went on to test the effects of systemically administered SKF81297 on the acquisition of trace conditioning. In experiment 3, SKF81297 was administered directly in prelimbic (PL) and infralimbic (IL) sub-regions of medial prefrontal cortex (mPFC) to compare the role of different mPFC sub-regions.

RESULTS

Whilst treatment with SCH23390 impaired motor responding and/or motivation, SKF81297 had relatively little effect in the pre-trained animals tested in experiment 1b. However, systemic SKF81297 depressed the acquisition function at the 2-s trace interval in experiment 2. Similarly, in experiment 3, SKF81297 (0.1 μg in 1.0 μl) microinjected into either PL or IL mPFC impaired appetitive conditioning at the 2-s trace interval.

CONCLUSIONS

Impaired trace conditioning under SKF81297 is likely to be mediated in part (but not exclusively) within the IL and PL mPFC sub-regions. The finding that trace conditioning was impaired rather than enhanced under SKF81297 provides further evidence for the inverse U-function which has been suggested to be characteristic of mPFC DA function.

摘要

理论依据

痕迹条件反射可能提供一种行为模型,适用于研究“在线”信息的维持及其潜在的神经基质。

目的

实验1a旨在通过缩短程序建立痕迹条件反射,该程序适合测试直接脑内微量注射多巴胺(DA)D1受体药物的效果。实验1b研究了在预先训练的动物中全身给药后DA D1激动剂SKF81297和DA D1拮抗剂SCH23390的效果。实验2继续测试全身给药的SKF81297对痕迹条件反射习得的影响。在实验3中,将SKF81297直接注射到内侧前额叶皮质(mPFC)的前边缘(PL)和下边缘(IL)子区域,以比较不同mPFC子区域的作用。

结果

虽然SCH23390治疗损害了运动反应和/或动机,但在实验1b中测试的预先训练的动物中,SKF81297的影响相对较小。然而,在实验2中,全身给予SKF81297在2秒痕迹间隔时抑制了习得功能。同样,在实验3中,将SKF81297(1.0μl中0.1μg)微量注射到PL或IL mPFC中,在2秒痕迹间隔时损害了食欲条件反射。

结论

SKF81297作用下痕迹条件反射受损可能部分(但非完全)由IL和PL mPFC子区域介导。在SKF81297作用下痕迹条件反射受损而非增强这一发现,为已被认为是mPFC DA功能特征的倒U型函数提供了进一步证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c8c/4502294/9e18bf1f4b48/213_2015_3903_Fig1_HTML.jpg

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