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Author Notes:

Email Address: Rosa M. Villalba : rvillal@emory.edu

The authors thank the Yerkes Center Animal Resources Division for help with the care of MPTP-treated monkeys.

Jean-Francois Pare and Susan Jenkins are also thanked for technical assistance.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Subjects:

Research Funding:

This work was supported by the-NIH grants R01NS083386, R01NS037948, the Udall Center grant P50NS071669-01 and the Yerkes Primate Center base grant P51-OD011132.

Keywords:

  • Parkinson’s disease
  • striatum
  • subthalamic nucleus
  • synaptic plasticity
  • glutamatergic synapses
  • vGluT
  • astrocytes plasticity

Morphological changes of glutamatergic synapses in animal models of Parkinson’s disease

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Journal Title:

Frontiers in Neuroanatomy

Volume:

Volume 9

Publisher:

Type of Work:

Article | Final Publisher PDF

Abstract:

The striatum and the subthalamic nucleus (STN) are the main entry doors for extrinsic inputs to reach the basal ganglia (BG) circuitry. The cerebral cortex, thalamus and brainstem are the key sources of glutamatergic inputs to these nuclei. There is anatomical, functional and neurochemical evidence that glutamatergic neurotransmission is altered in the striatum and STN of animal models of Parkinson’s disease (PD) and that these changes may contribute to aberrant network neuronal activity in the BG-thalamocortical circuitry. Postmortem studies of animal models and PD patients have revealed significant pathology of glutamatergic synapses, dendritic spines and microcircuits in the striatum of parkinsonians. More recent findings have also demonstrated a significant breakdown of the glutamatergic corticosubthalamic system in parkinsonian monkeys. In this review, we will discuss evidence for synaptic glutamatergic dysfunction and pathology of cortical and thalamic inputs to the striatum and STN in models of PD. The potential functional implication of these alterations on synaptic integration, processing and transmission of extrinsic information through the BG circuits will be considered. Finally, the significance of these pathological changes in the pathophysiology of motor and non-motor symptoms in PD will be examined.

Copyright information:

© 2015 Villalba, Mathai and Smith.

This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits making multiple copies, distribution, public display, and publicly performance, distribution of derivative works, provided the original work is properly cited. This license requires copyright and license notices be kept intact, credit be given to copyright holder and/or author.

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