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First published online 30 November 2005
doi: 10.1242/dev.02189

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Target-dependent specification of the neurotransmitter phenotype: cholinergic differentiation of sympathetic neurons is mediated in vivo by gp130 signaling

Matthias Stanke¹, Chi Vinh Duong¹, Manuela Pape¹, Markus Geissen^1,*, Guido Burbach², Thomas Deller², Hugues Gascan³, Rosanna Parlato⁴, Günther Schütz⁴ and Hermann Rohrer^1,

¹ Research Group Developmental Neurobiology, Max-Planck-Institute for Brain Research, Deutschordenstrasse 46, 60528 Frankfurt/M, Germany.
² Institute of Clinical Neuroanatomy, J.W.-Goethe University, Theodor-Stern-Kai 7, 60590 Frankfurt/M, Germany.
³ INSERM U564, CHU d'Angers, 4 rue Larrey, 49033 Angers Cedex, France.
⁴ Deptartment of Molecular Biology of the Cell I, German Cancer Research Center, Im Neuenheimer Feld 280, 69120 Heidelberg, Germany.

Author for correspondence (e-mail: rohrer{at}mpih-frankfurt.mpg.de)

Accepted 28 October 2005

Sympathetic neurons are generated through a succession of differentiation steps that initially lead to noradrenergic neurons innervating different peripheral target tissues. Specific targets, like sweat glands in rodent footpads, induce a change from noradrenergic to cholinergic transmitter phenotype. Here, we show that cytokines acting through the gp130 receptor are present in sweat glands. Selective elimination of the gp130 receptor in sympathetic neurons prevents the acquisition of cholinergic and peptidergic features (VAChT, ChT1, VIP) without affecting other properties of sweat gland innervation. The vast majority of cholinergic neurons in the stellate ganglion, generated postnatally, are absent in gp130-deficient mice. These results demonstrate an essential role of gp130-signaling in the target-dependent specification of the cholinergic neurotransmitter phenotype.

Key words: Cytokine, IL6/IL-6, Cholinergic, Sympathetic, VIP, VAChT

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