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Glutamate Plasticity in an Animal Model of Parkinson’s Disease

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Cortico-Subcortical Dynamics in Parkinson's Disease

Part of the book series: Contemporary Neuroscience ((CNEURO))

Although it is well established that in Parkinson’s disease there is a significant loss of dopamine within nerve terminals in the striatum, the depletion of dopamine most likely influences other neurotransmitter systems. There is growing interest in the interactions between dopamine and glutamate and it may be the lack of dopamine in Parkinson’s disease that results in dynamic changes in glutamate within at least the striatum [1, 2]. In the rodent, the sensorimotor cortex provides the primary excitatory, glutamatergic input to the dorsolateral striatum [3, 4], although recent data suggest that glutamate input from many nuclei within the thalamus may also be playing an important role [5–7]. The dopamine terminals originating from the substantia nigra pars compacta (SN-PC) make a symmetrical synaptic contact not only on the dendritic shaft of the medium spiny neuron but also on the neck of the dendritic spine [8, 9]. The asymmetrical synaptic contact on the head of that same spine within the dorsolateral striatum originates from not only the motor cortex but also the thalamus [5, 7] and the nerve terminals contain the neurotransmitter, glutamate [8, 10, 11]

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Acknowledgments

This research was supported by the Department of Veterans Affairs Merit Review Program. This work was carried out by a number of outstanding lab assistants over the past many years, including Cindy Moore, Justin Touchon, Carrie Nakamura, Jeffery Wiedemann, Modjgan Keyghobadi, Haley Holmer , Adrienne Tozier de la Poterie and graduate students, including Brenda McKee and Kristin McCarthy.

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Correspondence to Charles K. Meshul .

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Meshul, C.K. (2009). Glutamate Plasticity in an Animal Model of Parkinson’s Disease. In: Tseng, KY. (eds) Cortico-Subcortical Dynamics in Parkinson's Disease. Contemporary Neuroscience. Humana Press. https://doi.org/10.1007/978-1-60327-252-0_13

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