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Institute of Physiology and Pathophysiology

Calcium Imaging

The dynamics of the intracellular calcium concentration regulates a broad spectrum of cellular processes like cell motility and intracellular transduction neuronal and hormonal signals. A misregulation of calcium dynamics is involved in the genesis and pathophysiology of numerous deseases, e.g. calcium induced apoptosis.

 

In particular the dynamics of intracellular calcium ion channels (inositoltrisphosphate, IP3R and ryanodine receptor, RyR) can only be analysed with optical methods. These are based on calcium sensitive dyes (Fluo-4, Fura-2), which only fluoresce with calcium ions bound.

 

Elementary Calcium Release Events

The smallest events of intracellular calcium signaling are openings of single or small groups of calcium channels. These elementary calcium release events (ECRE or "sparks") have a spatial extension of less than 1-2 µm, which means they are only detectable with confocal laser scanning microscopes. The temporal extension is in the range of 10-200 ms so that time-resolved measurements are only possible by scanning a single line or very small frames.

 

Figure 1: Confocal linescan image of ECREs through RyR type 2 in cardiac muscle cells

 

This technique is applied to study the effects of physiological modulations and diverse anesthetics on the ryanodine receptor. The detection of ECREs was automated using specifically adapted image processing techniques.

 

Figure 2: Analysis of intracellular calcium dynamics in coupled HepG2 cell clusters

Calcium Oszillation

Oscillations of the intracellular calcium concentration are known as a way of signal transduction between cells. Changes in amplitude and frequency of these oscillations can induce cell proliferation or the growth of synapses in neuronal networks.

 

We study purine receptor-mediated calcium oscillations in cultured HepG2 carcinoma cells and the effects of anesthetics on the dynamics of calcium oscillations in cultured neurons.

 


Recent Publications

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Metabolic modulation of neuronal gamma-band oscillations. Pflugers Arch2018 Sep;470(9):1377-1389. doi: 10.1007/s00424-018-2156-6. Epub 2018 May 28.

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Electrical coupling between hippocampal neurons: contrasting roles of principal cell gap junctions and interneuron gap junctions. Cell Tissue Res. 2018 Aug 15. doi: 10.1007/s00441-018-2881-3. [Epub ahead of print] Review.

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Selective vulnerability of αOFF retinal ganglion cells during onset of autoimmune optic neuritis. Neuroscience. 2018 Jul 31. pii: S0306-4522(18)30515-3. doi: 10.1016/j.neuroscience.2018.07.040. [Epub ahead of print]

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Strategy for marker-based differentiation of pro- and anti-inflammatory macrophages using matrix-assisted laser desorption/ionization mass spectrometry imaging. Analyst. 2018 Jul 20. doi: 10.1039/c8an00659h. [Epub ahead of print]

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Improving electrical properties of iPSC-cardiomyocytes by enhancing Cx43 expression. J Mol Cell Cardiol. 2018 Jul;120:31-41. doi: 10.1016/j.yjmcc.2018.05.010. Epub 2018 May 16.

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Role of CD40 and ADAMTS13 in von Willebrand factor-mediated endothelial cell-platelet-monocyte interaction. Proc Natl Acad Sci U S A. 2018 Jun 12;115(24):E5556-E5565. doi: 10.1073/pnas.1801366115. Epub 2018 May 23.

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The VAMP-associated protein VAPB is required for cardiac and neuronal pacemaker channel function. FASEB J. 2018 Jun 7:fj201800246R. doi: 10.1096/fj.201800246R. [Epub ahead of print]

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Persistent sodium current modulates axonal excitability in CA1 pyramidal neurons. J Neurochem. 2018 Jun 4. doi: 10.1111/jnc.14479. [Epub ahead of print]

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The lncRNA CASC9 and RNA binding protein HNRNPL form a complex and co-regulate genes linked to AKT signaling. Hepatology. 2018 May 23. doi: 10.1002/hep.30102. [Epub ahead of print]

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Early Blood-Brain Barrier Disruption in Ischemic Stroke Initiates Multifocally Around Capillaries/Venules. Stroke. 2018 Jun;49(6):1479-1487. doi: 10.1161/STROKEAHA.118.020927. Epub 2018 May 14.

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Impact of carbonylation on glutathione peroxidase-1 activity in human hyperglycemic endothelial cells. Redox Biol. 2018 Jun;16:113-122. doi: 10.1016/j.redox.2018.02.018. Epub 2018 Mar 1.

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Endothelial progenitor cells accelerate endothelial regeneration in an in vitro model of Shigatoxin-2a-induced injury via soluble growth factors. Am J Physiol Renal Physiol. 2018 Mar 7. doi: 10.1152/ajprenal.00633.2017. [Epub ahead of print]


Institute of
Physiology and Pathophysiology

Heidelberg University

Im Neuenheimer Feld 326

69120 Heidelberg

Germany

Phone:+49 6221 54-4035
Fax:+49 6221 54-4038
E-mail:sekretariat.hecker@
physiologie.uni-heidelberg.de