Aberrant striatal plasticity is specifically associated with dyskinesia following levodopa treatment

Pauline Belujon, Daniel J. Lodge, Anthony A. Grace

Research output: Contribution to journalArticlepeer-review

38 Scopus citations

Abstract

Chronic levodopa treatment for Parkinson's disease often results in the development of abnormal involuntary movement, known as L-dopa-induced dyskinesia (LIDs). Studies suggest that LIDs may be associated with aberrant corticostriatal plasticity. Using in vivo extracellular recordings from identified Type I and Type II medium spiny striatal neurons, chronic L-dopa treatment was found to produce abnormal corticostriatal information processing. Specifically, after chronic L-dopa treatment in dopamine-depleted rats, there was a transition from a cortically evoked long-term depression (LTD) to a complementary but opposing form of plasticity, long-term potentiation, in Type II "indirect" pathway neurons. In contrast, LTD could still be induced in Type I neurons. Interestingly, the one parameter that correlated best with dyskinesias was the inability to de-depress established LTD in Type I medium spiny striatal neurons. Taken as a whole, we propose that the induction of LIDs is due, at least in part, to an aberrant induction of plasticity within the Type II indirect pathway neurons combined with an inability to de-depress established plastic responses in Type I neurons. Such information is critical for understanding the cellular mechanisms underlying one of the major caveats to L-dopa therapy.

Original languageEnglish (US)
Pages (from-to)1568-1576
Number of pages9
JournalMovement Disorders
Volume25
Issue number11
DOIs
StatePublished - Aug 15 2010

Keywords

  • Basal ganglia
  • Dopamine
  • Motor cortex
  • Parkinson's disease
  • Synaptic plasticity

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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