Current models of language processing do not address mechanisms at the neurotransmitter level, nor how pharmacologic agents may improve language function(s) in seemingly disparate disorders. L-Glutamate, the primary excitatory neurotransmitter in the human brain, is extensively involved in various higher cortical functions. We postulate that the physiologic role of L-Glutamate neurotransmission extends to the regulation of language access, comprehension, and production, and that disorders in glutamatergic transmission and circuitry contribute to the pathogenesis of neurodegenerative diseases and sporadic-onset language disorders such as the aphasic stroke syndromes. We start with a review of basic science data pertaining to various glutamate receptors in the CNS and ways that they may influence the physiological processes of language access and comprehension. We then focus on the dysregulation of glutamate neurotransmission in three conditions in which language dysfunction is prominent: Alzheimer’s Disease, Fragile X-associated Tremor/Ataxia Syndrome, and Aphasic Stroke Syndromes. Finally, we review the pharmacologic and electrophysiologic (event related brain potential or ERP) data pertaining to the role glutamate neurotransmission plays in language processing and disorders.

当前的语言处理模型没有解决神经递质水平的机制，也没有解决药物如何改善看似不同的疾病中的语言功能。 L-谷氨酸是人脑中主要的兴奋性神经递质，广泛参与各种高级皮质功能。我们假设 L-谷氨酸神经传递的生理作用延伸到语言获取、理解和产生的调节，并且谷氨酸传递和回路的障碍导致神经退行性疾病和散发性语言障碍（例如失语性中风）的发病机制综合症。我们首先回顾有关中枢神经系统中各种谷氨酸受体的基础科学数据以及它们可能影响语言获取和理解的生理过程的方式。然后，我们重点关注三种语言功能障碍突出的情况下谷氨酸神经传递的失调：阿尔茨海默病、脆性 X 相关震颤/共济失调综合征和失语性中风综合征。最后，我们回顾了与谷氨酸神经传递在语言处理和障碍中的作用有关的药理学和电生理学（事件相关脑电位或 ERP）数据。