Spatial working memory deficits and their relationship to negative symptoms in unmedicated schizophrenia patients
Spatial working memory deficits and their relationship to negative symptoms in unmedicated schizophrenia patients
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DOI：
10.1016/s0006-3223(96)00350-2
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发表时间：
1996-11-01
影响因子：
10.6
通讯作者：
OShoraCelaya, L
中科院分区：
文献类型：
--
作者：
Carter, C;Robertson, L;OShoraCelaya, L
近年来，病理学在涉及精神分裂症认知缺陷的背外侧前额叶皮质(DLPFC)的神经回路中的作用已被强调。特别是，在精神分裂症的认知缺陷和前额叶皮质主沟区域受损的非人类灵长类动物中观察到的工作记忆缺陷之间进行了类比(Goldman-Rakic 1987)。延迟期内该区域神经元的活动与眼球运动空间延迟反应任务中的准确表现有关。这种活动似乎依赖于儿茶酚胺能，特别是多巴胺能神经支配(Brozoski等人1979年；Sawaguchi和Goldman-Rakic 1991年)。这导致了一种精神分裂症认知缺陷的模型，其特征是前额叶背外侧皮质多巴胺能神经支配功能障碍，导致工作记忆功能受损。最近，Park和Holzman(1992)报告说，药物治疗的精神分裂症患者在人类模拟眼动延迟反应任务中表现出障碍，Goldman-Rakic在她对非人类灵长类动物的研究中使用了这种任务，以及触觉版本的任务。这一发现提供了一个重要的经验
A role for pathology in neural circuits involving the dorsolateral prefrontal cortex (DLPFC) underlying cognitive deficits in schizophrenia has been emphasized in the literature in recent years. In particular, analogies have been drawn between cognitive deficits seen in schizophrenia and working memory deficits observed in behaving nonhuman primates with lesions in the principal sulcal region of the prefrontal cortex (Goldman-Rakic 1987). Activity of neurons in this region during a delay period is associated with accurate performance during oculomotor spatial delayed response tasks. This activity appears dependent upon catecholaminergic, particularly dopaminergic innervation (Brozoski et al 1979; Sawaguchi and Goldman-Rakic 1991). This has led to a model of cognitive deficits in schizophrenia characterized by dysfunction in dopaminergic innervation in dorsolateral prefrontal cortex resulting in impaired working memory function.Recently, Park and Holzman (1992) reported that medicated schizophrenia patients showed impairment on a human analogue of the oculomotor delayed response task used by Goldman-Rakic in her studies of nonhuman primates, as well as on a haptic version of the task. This finding provided an important empirical