GDNF acutely modulates excitability and A-type K+ channels in midbrain dopaminergic neurons

Feng Yang, Linyin Feng, Bai Lu, Steven W. Johnson, Chien Ping Wu, Liya Shen

Research output: Contribution to journalArticlepeer-review

124 Scopus citations


Glial cell line-derived neurotrophic factor (GDNF) prevents lesion-induced death of midbrain dopaminergic neurons, but its function in normal brain remains uncertain. Here we show that GDNF acutely and reversibly potentiated the excitability of cultured midbrain neurons by inhibiting transient A-type K+ channels. The effects of GDNF were limited to large, tyrosine hydroxylase (TH)-positive dopaminergic neurons, and were mediated by mitogen associated protein (MAP) kinase. Application of GDNF also elicited a MAP kinase-dependent enhancement of the excitability in dopaminergic neurons in midbrain slice. These results demonstrate an acute regulation of GDNF on ion channels and its underlying signaling mechanism, and reveal an unexpected role of GDNF in normal midbrain dopaminergic neurons.

Original languageEnglish (US)
Pages (from-to)1071-1078
Number of pages8
JournalNature Neuroscience
Issue number11
StatePublished - 2001

ASJC Scopus subject areas

  • Neuroscience(all)


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