March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Acute Psychosocial Stress Protects Against Light-induced Damage Of Photoreceptors Via A Corticosterone-mediated Activation Of The Akt Pathway
Author Affiliations & Notes
  • Tembei K. Forkwa
    Human Anatomy and Embryology,
    University of Regensburg, Regensburg, Germany
  • Stefan Reber
    Department of Behavioral and Molecular Neuroendocrinology,
    University of Regensburg, Regensburg, Germany
  • Inga Neumann
    Department of Behavioral and Molecular Neuroendocrinology,
    University of Regensburg, Regensburg, Germany
  • Ernst Tamm
    Human Anatomy and Embryology,
    University of Regensburg, Regensburg, Germany
  • Andreas Ohlmann
    Human Anatomy and Embryology,
    University of Regensburg, Regensburg, Germany
  • Footnotes
    Commercial Relationships  Tembei K. Forkwa, None; Stefan Reber, None; Inga Neumann, None; Ernst Tamm, None; Andreas Ohlmann, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 2570. doi:https://doi.org/
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      Tembei K. Forkwa, Stefan Reber, Inga Neumann, Ernst Tamm, Andreas Ohlmann; Acute Psychosocial Stress Protects Against Light-induced Damage Of Photoreceptors Via A Corticosterone-mediated Activation Of The Akt Pathway. Invest. Ophthalmol. Vis. Sci. 2012;53(14):2570. doi: https://doi.org/.

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

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Abstract

Purpose: : Glucocorticoids have repeatedly been shown to be neuroprotective in animal models of hereditary retinal degenerations and glaucoma by inhibiting the apoptotic death of photoreceptors or retinal ganglion cells. Glucocorticoid release is one of the hallmarks of the classical stress response. To analyze if psychosocial stress has protective effects on retinal neurons, mice were stressed by subordinate colony housing (CSC) followed by a light-induced damage of photoreceptors. In addition, the roles of the HPA axis, Müller cell gliosis and AKT pathway activation in stress-mediated neuroprotection was investigated.

Methods: : Psychosocial stress was induced via subordinate colony housing (CSC) either for 10 hrs (acute stress) or 19 days (chronic stress). To induce photoreceptor degeneration Balb/c mice were exposed to 5000 lux white fluorescent light. Apoptosis and loss of photoreceptors were assessed by TUNEL staining and/or light microscopy. Corticosterone levels were measured by ELISA. To investigate the role of the HPA axis, adrenalectomy was performed. Retinal expression of neuroprotective growth factors and phosphorylation of AKT was analyzed by real-time RT-PCR and western blotting.

Results: : Acute psychosocial stress due to 10 hrs CSC housing protected photoreceptors from light induced damage when compared to single-housed controls, an effect that was lost after 19 days CSC housing. Injection of corticosterone (52mg/kg ip) was as effective in protecting photoreceptors from damage as was 10 hrs CSC housing. As opposed to those of sham-operated mice, photoreceptors of adrenalectomized mice were not protected from light damage after 10 hrs CSC, but showed an extremely high susceptibility to light damage. Retinal mRNA expression of neuroprotective factors (LIF, EDN-2, FGF-2, CNTF) was not changed after 10 hrs CSC or corticosterone injection when compared to SHC and vehicle-injected controls, respectively, both before and after light damage. After 10 hrs CSC or corticosterone injection, a significant higher level of Akt phoshorylation was observed when compared to single-housed controls or vehicle-injected animals. The same was true when sham-operated mice were compared with adrenalectomized mice.

Conclusions: : Acute psychosocial stress protects photoreceptors against light-induced damage. This effect is most likely mediated via an increase in plasma corticosterone which in turn activates the AKT signalling pathway.

Keywords: apoptosis/cell death • photoreceptors • cell survival 
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