Retailleau Aude, Boraud Thomas
Sagol Department of Neurobiology, University of Haifa Haifa, Israel.
Institut des Maladies Neurodegeneratives UMR 5293, University of Bordeaux Bordeaux, France ; Institut des Maladies Neurodegeneratives UMR 5293, CNRS Bordeaux, France.
Front Syst Neurosci. 2014 Mar 18;8:32. doi: 10.3389/fnsys.2014.00032. eCollection 2014.
Spatial learning has been recognized over the years to be under the control of the hippocampus and related temporal lobe structures. Hippocampal damage often causes severe impairments in the ability to learn and remember a location in space defined by distal visual cues. Such cognitive disabilities are found in Parkinsonian patients. We recently investigated the role of dopamine in navigation in the 6-Hydroxy-dopamine (6-OHDA) rat, a model of Parkinson's disease (PD) commonly used to investigate the pathophysiology of dopamine depletion (Retailleau et al., 2013). We demonstrated that dopamine (DA) is essential to spatial learning as its depletion results in spatial impairments. Our results showed that the behavioral effect of DA depletion is correlated with modification of the neural encoding of spatial features and decision making processes in hippocampus. However, the origin of these alterations in the neural processing of the spatial information needs to be clarified. It could result from a local effect: dopamine depletion disturbs directly the processing of relevant spatial information at hippocampal level. Alternatively, it could result from a more distributed network effect: dopamine depletion elsewhere in the brain (entorhinal cortex, striatum, etc.) modifies the way hippocampus processes spatial information. Recent experimental evidence in rodents, demonstrated indeed, that other brain areas are involved in the acquisition of spatial information. Amongst these, the cortex-basal ganglia (BG) loop is known to be involved in reinforcement learning and has been identified as an important contributor to spatial learning. In particular, it has been shown that altered activity of the BG striatal complex can impair the ability to perform spatial learning tasks. The present review provides a glimpse of the findings obtained over the past decade that support a dialog between these two structures during spatial learning under DA control.
多年来，空间学习一直被认为受海马体及相关颞叶结构的控制。海马体损伤常常会导致在学习和记忆由远处视觉线索所界定的空间位置方面的能力严重受损。帕金森病患者就存在这种认知障碍。我们最近在6-羟基多巴胺（6-OHDA）大鼠中研究了多巴胺在导航中的作用，该大鼠是帕金森病（PD）的一种模型，常用于研究多巴胺耗竭的病理生理学（雷塔约等人，2013年）。我们证明多巴胺（DA）对空间学习至关重要，因为其耗竭会导致空间功能受损。我们的研究结果表明，多巴胺耗竭的行为效应与海马体中空间特征的神经编码及决策过程的改变相关。然而，空间信息神经处理中这些改变的起源仍需阐明。这可能是局部效应导致的：多巴胺耗竭直接干扰了海马体水平上相关空间信息的处理。或者，也可能是更广泛的网络效应导致的：大脑其他部位（内嗅皮质、纹状体等）的多巴胺耗竭改变了海马体处理空间信息的方式。最近在啮齿动物中的实验证据确实表明，其他脑区也参与了空间信息的获取。其中，皮质-基底神经节（BG）环路已知参与强化学习，并已被确定为空间学习的一个重要促成因素。特别是，研究表明BG纹状体复合体的活动改变会损害执行空间学习任务的能力。本综述简要介绍了过去十年间获得的研究结果，这些结果支持在多巴胺控制下的空间学习过程中这两个结构之间存在相互作用。
