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

Paolo Calabresi, Francesca Galletti, Emanuele Saggese, Veronica Ghiglieri, Barbara Picconi

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
JournalParkinsonism and Related Disorders
Issue numberSUPPL. 3
Publication statusPublished - 2007


  • Basal ganglia
  • Dopamine
  • Long-term depression
  • Long-term potentiation
  • Sleep
  • Synaptic transmission

ASJC Scopus subject areas

  • Ageing
  • Clinical Neurology
  • Neurology


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