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Synaptic and cellular plasticity in Parkinson's disease.

Hong-Yuan Chu1,2

  • 1Center for Neurodegenerative Sciences, Van Andel Institute, Grand Rapids, MI, USA. hongyuan.chu@vai.org.

Acta Pharmacologica Sinica
|March 1, 2020
PubMed
Summary

Parkinson's disease involves the loss of dopamine neurons, leading to abnormal brain activity and motor symptoms. This review details cellular changes in the basal ganglia that contribute to these pathological brain patterns.

Keywords:
Parkinson’s diseasebasal gangliadopaminestriatumsubthalamic nucleussynaptic plasticity

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Area of Science:

  • Neuroscience
  • Neurology
  • Cellular Biology

Background:

  • Parkinson's disease (PD) is a progressive neurodegenerative disorder.
  • It imposes a significant socioeconomic burden and causes debilitating motor and non-motor symptoms.
  • The cardinal motor symptoms are linked to the loss of dopaminergic neurons in the substantia nigra pars compacta.

Purpose of the Study:

  • To review recent advances in understanding synaptic and cellular alterations in the basal ganglia following dopamine loss.
  • To explore the conceptual understanding of cellular and circuit bases for pathological brain activity in Parkinson's disease.

Main Methods:

  • Review of accumulating evidence on cellular and synaptic changes.
  • Focus on alterations in the striatum and subthalamic nucleus.
  • Conceptual analysis of circuit activity in the parkinsonian state.

Main Results:

  • Dopamine depletion induces adaptive cellular and synaptic changes in the basal ganglia.
  • These adaptations contribute to abnormal, rhythmic activity patterns in the cortico-basal ganglia-thalamocortical network.
  • Pathological brain activity patterns are closely associated with PD motor symptoms.

Conclusions:

  • Both dopaminergic degeneration and abnormal basal ganglia circuit activity drive Parkinson's disease motor symptoms.
  • Understanding these cellular and circuit alterations is crucial for comprehending PD pathophysiology.
  • Further research into these mechanisms may offer therapeutic insights.