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Brain Plast. 2015;1(1):29-39.

The Effects of Exercise on Dopamine Neurotransmission in Parkinson's Disease: Targeting Neuroplasticity to Modulate Basal Ganglia Circuitry.

Author information

1
Department of Neurology, University of Southern California, Los Angeles, CA, 90033 ; Division of Biokinesiology and Physical Therapy, University of Southern California, Los Angeles, CA, 90033.
2
Department of Neurology, University of Southern California, Los Angeles, CA, 90033 ; Department of Psychiatry and the Behavioral Sciences, University of Southern California, Los Angeles, CA, 90033.
3
Andrus Gerontology, University of Southern California, Los Angeles, CA, 90033, and Department of Psychiatry & Biobehavioral Sciences, University of California at Los Angeles, Los Angeles, CA, 90095.
4
Department of Neurology, University of Southern California, Los Angeles, CA, 90033.
5
Department of Psychology, CUNY, New York.

Abstract

Animal studies have been instrumental in providing evidence for exercise-induced neuroplasticity of corticostriatal circuits that are profoundly affected in Parkinson's disease. Exercise has been implicated in modulating dopamine and glutamate neurotransmission, altering synaptogenesis, and increasing cerebral blood flow. In addition, recent evidence supports that the type of exercise may have regional effects on brain circuitry, with skilled exercise differentially affecting frontal-striatal related circuits to a greater degree than pure aerobic exercise. Neuroplasticity in models of dopamine depletion will be reviewed with a focus on the influence of exercise on the dorsal lateral striatum and prefrontal related circuitry underlying motor and cognitive impairment in PD. Although clearly more research is needed to address major gaps in our knowledge, we hypothesize that the potential effects of exercise on inducing neuroplasticity in a circuit specific manner may occur through synergistic mechanisms that include the coupling of an increasing neuronal metabolic demand and increased blood flow. Elucidation of these mechanisms may provide important new targets for facilitating brain repair and modifying the course of disease in PD.

KEYWORDS:

basal ganglia; cognition; glutamate; prefrontal cortex; synaptic plasticity

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