Dopamine controls neurogenesis in the adult salamander midbrain in homeostasis and during regeneration of dopamine neurons

Daniel A. Berg, Matthew Kirkham, Heng Wang, Jonas Frisén, András Simon*

*Corresponding author for this work

Research output: Contribution to journalArticle

48 Citations (Scopus)

Abstract

Appropriate termination of regenerative processes is critical for producing the correct number of cells in tissues. Here we provide evidence for an end-product inhibition of dopamine neuron regeneration that is mediated by dopamine. Ablation of midbrain dopamine neurons leads to complete regeneration in salamanders. Regeneration involves extensive neurogenesis and requires activation of quiescent ependymoglia cells, which express dopamine receptors. Pharmacological compensation for dopamine loss by L-dopa inhibits ependymoglia proliferation and regeneration in a dopamine receptor-signaling-dependent manner, specifically after ablation of dopamine neurons. Systemic administration of the dopamine receptor antagonist haloperidol alone causes ependymoglia proliferation and the appearance of excessive number of neurons. Our data show that stem cell quiescence is under dopamine control and provide a model for termination once normal homeostasis is restored. The findings establish a role for dopamine in the reversible suppression of neurogenesis in the midbrain and have implications for regenerative strategies in Parkinson's disease.

Original languageEnglish
Pages (from-to)426-433
Number of pages8
JournalCell Stem Cell
Volume8
Issue number4
DOIs
Publication statusPublished - 8 Apr 2011

ASJC Scopus subject areas

  • Molecular Medicine
  • Genetics
  • Cell Biology

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