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Neurotransmitter phenotype-specific expression changes in developing sympathetic neurons.

Galina Apostolova1, Roland Dorn, Sojeong Ka

  • 1Institute for Neuroscience, Innsbruck Medical University, MZA, Anichstrasse 35, 6020 Innsbruck, Austria.

Molecular and Cellular Neurosciences
|May 22, 2007
PubMed
Summary
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Sympathetic neurons switch neurotransmitters during development. Neurotrophic factors trigger this change, with bone morphogenetic protein signaling identified as an inhibitor of cholinergic differentiation.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Developmental Biology

Background:

  • Sympathetic neurons exhibit plasticity, switching from noradrenergic to cholinergic neurotransmission during late development.
  • This neurotransmitter switch is influenced by target-derived signals in vivo and neurotrophic factors in vitro.

Purpose of the Study:

  • To analyze genome-wide gene expression differences between noradrenergic and cholinergic sympathetic neuron phenotypes.
  • To identify genes and signaling pathways involved in the developmental neurotransmitter switch.

Main Methods:

  • Utilized DNA microarrays to profile RNA expression in chick sympathetic ganglia.
  • Treated neurons with neurotrophin 3, glial cell line-derived neurotrophic factor, ciliary neurotrophic factor, and nerve growth factor.

Related Experiment Videos

  • Compared gene expression profiles to define noradrenergic and cholinergic synexpression groups.

    • Main Results:

    • Identified distinct gene sets associated with noradrenergic and cholinergic neurotransmission.
    • Found enrichment in functional categories including signal transduction, G-protein-coupled signaling, cation transport, neurogenesis, and synaptic transmission.
    • Discovered that bone morphogenetic protein signaling inhibits cholinergic differentiation.

    Conclusions:

    • Genome-wide expression analysis reveals key molecular players in sympathetic neuron neurotransmitter plasticity.
    • Bone morphogenetic protein signaling acts as a crucial regulator, inhibiting the switch to cholinergic neurotransmission.