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J Neural Transm (Vienna). 2018 Mar;125(3):449-460. doi: 10.1007/s00702-017-1744-5. Epub 2017 Jun 15.

Dysregulation of striatal projection neurons in Parkinson's disease.

Author information

1
Yerkes National Primate Research Center, Emory University, 954 Gatewood Road, Atlanta, GA, 30329, USA.
2
Yerkes National Primate Research Center, Emory University, 954 Gatewood Road, Atlanta, GA, 30329, USA. spapa@emory.edu.
3
Department of Neurology, Emory University School of Medicine, Atlanta, GA, 30329, USA. spapa@emory.edu.

Abstract

The loss of nigrostriatal dopamine (DA) is the primary cause of motor dysfunction in Parkinson's disease (PD), but the underlying striatal mechanisms remain unclear. In spite of abundant literature portraying structural, biochemical and plasticity changes of striatal projection neurons (SPNs), in the past there has been a data vacuum from the natural human disease and its close model in non-human primates. Recently, single-cell recordings in advanced parkinsonian primates have generated new insights into the altered function of SPNs. Currently, there are also human data that provide direct evidence of profoundly dysregulated SPN activity in PD. Here, we review primate recordings that are impacting our understanding of the striatal dysfunction after DA loss, particularly through the analysis of physiologic correlates of parkinsonian motor behaviors. In contrast to recordings in rodents, data obtained in primates and patients demonstrate similar major abnormalities of the spontaneous SPN firing in the alert parkinsonian state. Furthermore, these studies also show altered SPN responses to DA replacement in the advanced parkinsonian state. Clearly, there is yet much to learn about the striatal discharges in PD, but studies using primate models are contributing unique information to advance our understanding of pathophysiologic mechanisms.

KEYWORDS:

Direct and indirect pathways; Dyskinesia; Non-human primates; Parkinson’s disease; Striatal projection neurons

PMID:
28620834
DOI:
10.1007/s00702-017-1744-5

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