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Related Concept Videos

The Retina01:32

The Retina

The retina is a layer of nervous tissue at the back of the eye that transduces light into neural signals. This process, called phototransduction, is carried out by rod and cone photoreceptor cells in the back of the retina.

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Class 5 transmembrane semaphorins control selective Mammalian retinal lamination and function.

Ryota L Matsuoka1, Onanong Chivatakarn, Tudor C Badea

  • 1The Solomon H. Snyder Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

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|August 13, 2011
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Transmembrane semaphorins Sema5A and Sema5B, along with PlexinA1 and PlexinA3 receptors, are crucial for correctly layering retinal neurons. Their absence in mice causes neurite mistargeting and functional deficits in the retina.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Developmental Biology

Background:

  • Retinal lamination is essential for vision, with neuronal processes confined to specific layers.
  • Mechanisms segregating neurites within the inner plexiform layer (IPL) remain largely unknown.

Purpose of the Study:

  • To investigate the role of transmembrane semaphorins in regulating retinal neurite targeting within the IPL.
  • To identify the specific semaphorin ligands and plexin receptors involved in inner retinal lamination.

Main Methods:

  • Utilized Sema5A and Sema5B knockout mouse models (Sema5A⁻/⁻; Sema5B⁻/⁻).
  • Examined neurite targeting of retinal ganglion cells (RGCs), amacrine, and bipolar cells.
  • Performed in vitro and in vivo experiments to assess neurite outgrowth inhibition via PlexinA1 and PlexinA3 receptors.

Main Results:

  • Sema5A and Sema5B were found to constrain neurites from multiple retinal neuron subtypes within the IPL.
  • Absence of Sema5A and Sema5B led to severe neurite mistargeting into outer retinal regions.
  • Targeting defects were pronounced in the outer (OFF) IPL layers, causing functional deficits in RGC responses.

Conclusions:

  • Sema5A and Sema5B act as key inhibitors of retinal neurite outgrowth, mediated by PlexinA1 and PlexinA3 receptors.
  • These semaphorin-plexin interactions are vital for establishing correct inner retinal lamination and function.
  • Defects in this system lead to aberrant neural circuitry and impaired visual processing.