Neuronal networks and synaptic plasticity in Parkinson's disease: beyond motor deficits

Parkinsonism Relat Disord. 2007:13 Suppl 3:S259-62. doi: 10.1016/S1353-8020(08)70013-0.

Abstract

The excitatory corticostriatal pathway, which plays a critical role in the building up and storage of adaptive motor behaviours, can undergo long-lasting, activity-dependent changes in the efficacy of synaptic transmission, named long-term potentiation (LTP) and long- term depression (LTD). Both forms of plasticity are thought to underlie motor learning and depend upon the concomitant activation of glutamatergic corticostriatal and dopaminergic nigrostriatal pathways. Accordingly, corticostriatal LTP and LTD are altered in Parkinson's Disease (PD) models. The dopamine (DA)/acetylcholine(Ach) synaptic unbalance could be responsible of some of the cognitive deficits described in PD patients. The impairment of DA/ACh-dependent cellular learning could lead to the storage of unessential memory traces, as it has been postulated for the induction of L-DOPA-induced dyskinesias. Other non-motor symptoms involve not only the central dopaminergic system, but also in the noradrenergic, serotoninergic and cholinergic transmitter systems.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Humans
  • Models, Biological
  • Movement Disorders / etiology
  • Movement Disorders / physiopathology
  • Nerve Net / physiopathology*
  • Neuronal Plasticity / physiology*
  • Parkinson Disease / complications
  • Parkinson Disease / pathology
  • Parkinson Disease / physiopathology*
  • Synapses / physiology