Paradoxical facilitation after depotentiation protocol can precede dyskinesia onset in early Parkinson’s disease

Research output: Contribution to journalArticle


  • Viviana Ponzo
  • Sonia Benitez-Rivero
  • Miguel Fernandez Del-Olmo
  • Michele Hu
  • Giacomo Koch
  • Binith Cheeran

External organisations

  • Nuffield Department of Clinical Neurosciences
  • Fondazione Santa Lucia
  • University of A Coruña
  • University of Rome Tor Vergata


Loss of dopamine, a key modulator of synaptic signalling, and subsequent pulsatile non-physiological levodopa replacement is believed to underlie altered neuroplasticity in Parkinson’s disease (PD). Animal models suggest that maladaptive plasticity (e.g. deficient depotentiation at corticostriatal synapses) is key in the development of levodopa-induced dyskinesia (LID), a common complication following levodopa replacement in PD. Human studies using transcranial magnetic stimulation protocols have shown similar depotentiation deficit in patients with LID. We hypothesized that subtle depotentiation deficits should precede LID if these deficits are mechanistically linked to LID onset. Moreover, patients on pulsatile levodopa-based therapy may show these changes earlier than those treated with levodopa-sparing strategies. We recruited 22 early non-dyskinetic PD patients (


Original languageEnglish
Pages (from-to)1-9
Number of pages9
JournalExperimental Brain Research
Early online date26 Aug 2016
Publication statusE-pub ahead of print - 26 Aug 2016


  • Depotentiation, Levodopa-induced dyskinesia, Parkinson’s disease, Potentiation, Synaptic plasticity

ASJC Scopus subject areas