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Munc18 and Munc13 regulate early neurite outgrowth.

Jurjen H P Broeke1, Martijn Roelandse, Maartje J Luteijn

  • 1Department of Functional Genomics, Vrije Universiteit (VU) and VU Medical Center (VUmc), Amsterdam, The Netherlands.

Biology of the Cell
|May 26, 2010
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Vesicle fusion proteins Munc18 and Munc13 are crucial for early neuronal outgrowth speed. Impaired fusion slows growth and alters growth cone shape, but this effect diminishes after synaptogenesis.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Developmental Biology

Background:

  • Neuronal growth cones utilize vesicular secretion proteins like SNAREs, Munc13, and Munc18.
  • Vesicle fusion in growth cones may facilitate neuronal outgrowth before synapse formation.

Purpose of the Study:

  • To investigate the role of vesicle fusion proteins (Munc18-1, Munc13-1/2) in neuronal outgrowth.
  • To determine if impaired vesicle fusion affects neurite outgrowth speed and growth cone morphology.

Main Methods:

  • Utilized dissociated cell and organotypic slice cultures from Munc18-1 null and Munc13-1/2 double null mice.
  • Assessed neurite length and growth cone filopodia during early development (DIV1-4) and after synaptogenesis (DIV14-23).

Main Results:

  • Release-deficient neurons exhibited decreased outgrowth speed and reduced total neurite length in early development.
  • Munc18-1 null neurons showed increased filopodia, unlike wild-type or Munc13-1/2 double null neurons.
  • The reduction in neurite length was not observed after synaptogenesis.

Conclusions:

  • Vesicle fusion is critical for initial neuronal outgrowth but not essential during or after synaptogenesis.
  • Outgrowth speed may not be rate-limiting for neuronal network formation in vitro.
  • Munc18, but not Munc13, regulates growth cone filopodia, potentially through actin dynamics.