Adrenergic activation attenuates astrocyte swelling induced by hypotonicity and neurotrauma

Nina Vardjan, Anemari Horvat, Jamie E. Anderson, Dou Yu, Deborah Croom, Xiang Zeng, Zala Lužnik, Marko Kreft, Yang D. Teng, Sergei A. Kirov, Robert Zorec*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

44 Scopus citations

Abstract

Edema in the central nervous system can rapidly result in life-threatening complications. Vasogenic edema is clinically manageable, but there is no established medical treatment for cytotoxic edema, which affects astrocytes and is a primary trigger of acute post-traumatic neuronal death. To test the hypothesis that adrenergic receptor agonists, including the stress stimulus epinephrine protects neural parenchyma from damage, we characterized its effects on hypotonicity-induced cellular edema in cortical astrocytes by in vivo and in vitro imaging. After epinephrine administration, hypotonicity-induced swelling of astrocytes was markedly reduced and cytosolic 3'-5'-cyclic adenosine monophosphate (cAMP) was increased, as shown by a fluorescence resonance energy transfer nanosensor. Although, the kinetics of epinephrine-induced cAMP signaling was slowed in primary cortical astrocytes exposed to hypotonicity, the swelling reduction by epinephrine was associated with an attenuated hypotonicity-induced cytosolic Ca2+ excitability, which may be the key to prevent astrocyte swelling. Furthermore, in a rat model of spinal cord injury, epinephrine applied locally markedly reduced neural edema around the contusion epicenter. These findings reveal new targets for the treatment of cellular edema in the central nervous system. GLIA 2016;64:1034-1049 Main Points: Epinephrine reduces hypotonic astrocyte swelling in vitro and in vivo. Cell swelling reduction involves cAMP-mediated Ca2+ hypoexcitability. Epinephrine reduces trauma-induced astrocyte swelling; a new possibility for the treatment of cellular edema.

Original languageEnglish (US)
Pages (from-to)1034-1049
Number of pages16
JournalGlia
Volume64
Issue number6
DOIs
StatePublished - Jun 1 2016

Funding

We thank Dr. Martin Lohse and Dr. Viacheslav Olegowitsch Nikolaev (University of Würzburg, Würzburg, Germany) for providing the Epac1-camps FRET plasmid construct. We also thank Ursa Gubensek for assistance with the experiments. This work was supported by the Slovenian Research Agency (P3 310 to R.Z., J3 4051 to R.Z., J3 3632 to R.Z., J3 6790 to R.Z., J3 4146 to M.K.), the Centre of Excellence for Integrated Approaches in Chemistry and Biology of Proteins to R.Z., the COST Action BM1002 to R.Z., the EduGlia ITN EU grant to R.Z., the National Institute of Health (NS083858 to S.A.K.), the American Heart Association (12GRNT16570006 to S.A.K.), the US Department of Veterans Affairs Rehabilitation Research and Development (B7076R to Y.D.T.), and the US Department of Defense- Center for Integration of Medicine & Innovative Technology grants to Y.D.T.

Keywords

  • Astrocytes
  • Cerebral cortex
  • Contusion trauma
  • Cytotoxic edema
  • Epinephrine
  • Spinal cord

ASJC Scopus subject areas

  • Neurology
  • Cellular and Molecular Neuroscience

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