April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
CaMKII Signaling Is Contributive To Neuritogenesis In Light-Induced Retinal Degeneration
Author Affiliations & Notes
  • Yanhua Lin
    Ophthalmology, John A Moran Eye Center, Salt Lake City, Utah
  • Bryan W. Jones
    Ophthalmology, John A Moran Eye Center, Salt Lake City, Utah
  • Kevin Rapp
    Ophthalmology, John A Moran Eye Center, Salt Lake City, Utah
  • Marguerite Shaw
    Ophthalmology, John A Moran Eye Center, Salt Lake City, Utah
  • Jia-Hui Yang
    Ophthalmology, John A Moran Eye Center, Salt Lake City, Utah
  • Carl B. Watt
    Ophthalmology, John A Moran Eye Center, Salt Lake City, Utah
  • Robert E. Marc
    Ophthalmology, John A Moran Eye Center, Salt Lake City, Utah
  • Footnotes
    Commercial Relationships  Yanhua Lin, None; Bryan W. Jones, None; Kevin Rapp, None; Marguerite Shaw, None; Jia-Hui Yang, None; Carl B. Watt, None; Robert E. Marc, None
  • Footnotes
    Support  NIH grant EY015128-04
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 1846. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Yanhua Lin, Bryan W. Jones, Kevin Rapp, Marguerite Shaw, Jia-Hui Yang, Carl B. Watt, Robert E. Marc; CaMKII Signaling Is Contributive To Neuritogenesis In Light-Induced Retinal Degeneration. Invest. Ophthalmol. Vis. Sci. 2011;52(14):1846.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

Purpose: : Retinal degenerations (RD), such as age-related macular degeneration (AMD) and retinitis pigmentosa (RP), lead to primary loss of photoreceptors and secondary remodeling of the surviving retina. A striking feature of remodeling is neuritogenesis, while the initiators of this process remain unknown. We hypothesize that Ca2+/calmodulin-dependent protein kinase II (CaMKII) signaling may influence the evolution of neuritogenesis and subsequent retinal remodeling.

Methods: : Adult albino mice were exposed to constant intense light (24 h) by excluding one normal night cycle (12 h) to establish the light-induced retinal degeneration (LIRD) animal model. Retinas were harvested at post-light exposure day (pLX) for CaMKII signaling analysis with morphological, metabolic profiling and biochemical parameters.

Results: : αCaMKII and βCaMKII were expressed in the neural retina. Low intracellular Ca2+ is known to favor expression of βCaMKII over αCaMKII, and our results showed that light stress immediately increased the protein levels of βCaMKII, but αCaMKII levels showed no change. Increase in βCaMKII/αCaMKII protein ratio correlated with elevated levels of Ca2+-impermeable AMPAR subunit GluR2 and with no change in highly Ca2+-permeable AMPAR subunit GluR1 expression. Inhibitor of CaMKII kinase activity (KN-62) accelerated neuritogenesis while antagonist of AMPAR (NBQX) mitigated neuritogenesis compared with LIRD retina. These changes were followed by bipolar cell neuritogenesis revealed by PKCα staining in the survivor zone.

Conclusions: : Even though the gross histology of the neural retina in the survivor zone seems normal early in LIRD, alterations to the fine dendritic circuitry in fact are underway. CaMKII signaling displays large alterations, suggesting potential CaMKII signaling and post-synaptic Ca2+ are responsible for neuritogenesis and reactive neuronal plasticity.

Keywords: retinal degenerations: cell biology • signal transduction: pharmacology/physiology • bipolar cells 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×