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Brain Res. 2014 Mar 13;1552:34-40. doi: 10.1016/j.brainres.2013.12.035. Epub 2014 Jan 4.

Cortical glutamate levels decrease in a non-human primate model of dopamine deficiency.

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Department of Neurosurgery, Xuan Wu Hospital, Capital Medical University, Beijing 100053, PR China.
Department of Anatomy and Neurobiology, University of Kentucky Chandler Medical Center, Lexington, KY 40536 0098 USA.
Department of Physiology, Key Laboratory for Neurodegenerative Disorders of the Ministry Education, Capital Medical University, Beijing 100069 China.
Magnetic Resonance Imaging and Spectroscopy Center, University of Kentucky Chandler Medical Center, Lexington, KY 40536-0098 USA.
Center for Microelectrode Technology, University of Kentucky Chandler Medical Center, Lexington, KY 40536-0098 USA.
Contributed equally


While Parkinson's disease is the result of dopaminergic dysfunction of the nigrostriatal system, the clinical manifestations of Parkinson's disease are brought about by alterations in multiple neural components, including cortical areas. We examined how 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration affected extracellular cortical glutamate levels by comparing glutamate levels in normal and MPTP-lesioned nonhuman primates (Macaca mulatta). Extracellular glutamate levels were measured using glutamate microelectrode biosensors. Unilateral MPTP-administration rendered the animals with hemiparkinsonian symptoms, including dopaminergic deficiencies in the substantia nigra and the premotor and motor cortices, and with statistically significant decreases in basal glutamate levels in the primary motor cortex on the side ipsilateral to the MPTP-lesion. These results suggest that the functional changes of the glutamatergic system, especially in the motor cortex, in models of Parkinson's disease could provide important insights into the mechanisms of this disease.


Cortical; Glutamate; MPTP; Microelectrode array; Parkinson's

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