Developmental changes in the expression level of connexin36 in the rat retina

Tamás Kovács-Öller1, Katalin Raics, József Orbán

  • 1Department of Experimental Zoology and Neurobiology, University of Pécs, Pécs, Ifjúság street 6, Hungary.

Cell and Tissue Research
|August 12, 2014
PubMed

Insights

Connexin36 (Cx36) gap junctions form in the developing rat retina, with expression and plaque formation increasing from birth to P20. Cx36 plaques show a preference for the ON sublamina and associate with AII amacrine cells, reflecting electrical circuit development.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Ophthalmology

Background:

  • Connexin36 (Cx36) is the primary gap junction protein in the brain and retina.
  • Retinal structural development involves significant changes in gap junction formation before functional circuits are established.

Purpose of the Study:

  • To investigate the temporal and spatial formation of inner retinal gap junctions by examining Cx36 expression during postnatal development.
  • To understand the role of Cx36 in the maturation of retinal electrical synaptic circuitry.

Main Methods:

  • Analysis of Cx36 mRNA and protein levels in rat retinas from postnatal day 0 (P0) to P20.
  • Immunohistochemical localization of Cx36 plaques in the inner plexiform layer (IPL).
  • Colocalization studies with calretinin-positive (CaR(+)) fibers and parvalbumin-positive (PV(+)) AII amacrine cells.

Main Results:

  • Cx36 transcript and protein expression continuously increased from P0 to P20.
  • Cx36 plaque formation began around P10 in the IPL, with a distinct preference for the ON sublamina.
  • Cx36 plaques were found to colocalize with AII amacrine cell dendrites, with specific stratification patterns emerging over time.

Conclusions:

  • Cx36 expression and localization in the developing rat IPL follow a specific sequence, mirroring the formation of electrical synaptic circuits.
  • The observed Cx36 changes are attributed to the formation of gap junctions between AII amacrine cells and ON cone bipolar cells, and subsequently between AII amacrine cells themselves.

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