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DSCAM and DSCAML1 function in self-avoidance in multiple cell types in the developing mouse retina.

Peter G Fuerst1, Freyja Bruce, Miao Tian

  • 1The Jackson Laboratory, Bar Harbor, ME 04609, USA.

Neuron
|December 1, 2009
PubMed
Summary
This summary is machine-generated.

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Down syndrome cell adhesion molecule (DSCAM) and DSCAM-LIKE1 (DSCAML1) are crucial for neuronal self-avoidance in the developing mouse retina. These genes ensure proper dendritic and cell body spacing but are not essential for synaptic specificity.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Retinal Circuitry

Background:

  • Down syndrome cell adhesion molecule (DSCAM) and DSCAM-LIKE1 (DSCAML1) are known to play roles in neuronal development, including axon guidance and synaptic adhesion.
  • Their specific functions in the developing mammalian retina, particularly concerning neuronal self-avoidance and synaptic specificity, require further elucidation.

Purpose of the Study:

  • To investigate the roles of DSCAM and DSCAML1 in the developing mouse retina.
  • To determine if DSCAM and DSCAML1 are essential for neuronal self-avoidance and synaptic specificity in retinal ganglion cells (RGCs) and the rod circuit.

Main Methods:

  • Utilized knockout mouse models (Dscam(-/-) and Dscaml1(-/-)) to study gene function.
  • Examined retinal morphology, including dendritic fasciculation and cell body clustering, using microscopy.

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  • Assessed neuronal stratification and synapse formation in the inner plexiform layer.

    • Main Results:

    • Dscam deficiency in mice led to fasciculated dendrites and clumped cell bodies in retinal ganglion cells (RGCs), indicating a role in RGC self-avoidance.
    • Dscaml1 deficiency resulted in fasciculated rod bipolar cell dendrites and clumped AII amacrine cell bodies, also suggesting a role in self-avoidance within the rod circuit.
    • Despite defects in self-avoidance, neuronal processes stratified correctly, and functional synapses formed in the Dscaml1 mutant retina.

    Conclusions:

    • DSCAM and DSCAML1 function analogously in mediating neuronal self-avoidance in the developing mouse retina.
    • Neither DSCAM nor DSCAML1 appears to be essential for establishing synaptic specificity within the studied retinal circuits.
    • These findings highlight the conserved role of DSCAM family members in preventing neuronalprocess overlap during development.