Membrane Excitability and Cellular Calcium Regulation in the peripheral Nervous System under different (patho)-physiological Conditions and in Inflammatory Disease

FAU-externes Projekt

Details zum Projekt

Prof. Dr. Dr. Oliver Friedrich

Beteiligte FAU-Organisationseinheiten:
Lehrstuhl für Medizinische Biotechnologie

Akronym: ARC International Linkage Fellowship
Projektstart: 01.04.2008
Projektende: 31.03.2009

Abstract (fachliche Beschreibung):

The applicant aims to perform electrophysiology and fluorescence microscopy experiments in mammalian neurons and skeletal muscle cells under
(patho-)physiological conditions. Cellular Ca2+ and membrane potential signaling are investigated with high resolution confocal microscopy or ultrafast CCD cameras while electrically stimulating cells. In cellular models of severe inflammation and sepsis, cytokines will be applied to cells and changes in signaling studied. We expect that Ca2+ and membrane signals are impaired under these conditions. This will clarify mechanisms underlying organ failure of nervous system in critical illness that is among the top death counts. Therefore, this research will be of high significance.

The objectives were to study cellular Ca2+ signalling and ion channel functions under pathophysiological situations related to human disorders, mainly in skeletal muscle and peripheral neurons.

1.    Ca2+ homeostasis was meant to be studied under conditions of inflammatory cytokine load as a model for sepsis related myopathy (own project and collaboration with PI Launikonis).
2.    Ion channel function of the surface membrane was meant to be studied under conditions with altered membrane cholesterol composition that could be important for treatment of obesity (collaboration with PI Launikonis).
3.    Cellular Ca2+ responses to store depletion in muscular dystrophy (collaboration with PI Launikonis)
4.    Regulation of Ca2+ homeostasis in skeletal muscle by mechanosensitive channels under (patho-)physiological conditions (collaboration PI Martinac)
5.    It was planned to establish a combined fluorescence method to study membrane potential and Ca2+ fluctuations in peripheral neurons and apply this to inflammatory disease (collaboration PI Adams)

Externe Partner

Queensland University of Technology (QUT)


Edwards, J.N., Weber, C., Liu, I., Reischl, B., Most, P., Wirth-Hücking, A.,... Cully, T.R. (2014). IL-1α reversibly inhibits skeletal muscle ryanodine receptor a novel mechanism for critical illness myopathy? American journal of respiratory cell and molecular biology, 50(6), 1096-1106.
Friedrich, O., Hund, E., & von Wegner, F. (2010). Enhanced muscle shortening and impaired Ca2+ channel function in an acute septic myopathy model. Journal of neurology, 257(4), 546-55.
Friedrich, O., Fink, R., & von Wegner, F. (2010). New factors contributing to dynamic calcium regulation in the skeletal muscle triad-a crowded place. Biophysical Reviews, 2(1), 29-38.
Edwards, J.N., Murphy, R.M., Cully, T.R., von Wegner, F., Friedrich, O., & Launikonis, B.S. (2010). Ultra-rapid activation and deactivation of store-operated Ca(2+) entry in skeletal muscle. Cell calcium, 47(5), 458-67.
Edwards, J.N., Friedrich, O., Cully, T.R., von Wegner, F., Murphy, R.M., & Launikonis, B.S. (2010). Upregulation of store-operated Ca2+ entry in dystrophic mdx mouse muscle. American journal of physiology. Cell physiology, 299(1), C42-50.
Teichmann, M.D.H., von Wegner, F., Fink, R., Chamberlain, J.S., Launikonis, B.S., Martinac, B., & Friedrich, O. (2008). Inhibitory control over Ca(2+) sparks via mechanosensitive channels is disrupted in dystrophin deficient muscle but restored by mini-dystrophin expression. PLoS ONE, 3(11), e3644.

Zuletzt aktualisiert 2019-28-06 um 22:47