Select languageSelect language
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

*

Astrocytic glutamine synthetase is expressed in the neuronal somatic layers and down-regulated proportionally to neuronal loss in the human epileptic hippocampus. Glia. 2018 Jan 19. doi: 10.1002/glia.23292. [Epub ahead of print]

*

Modulation of glutathione peroxidase activity by age-dependent carbonylation in glomeruli of diabetic mice. J Diabetes Complications. 2018 Feb;32(2):130-138. doi: 10.1016/j.jdiacomp.2017.11.007. Epub 2017 Nov 22.

*

Sensitive mass spectrometric assay for determination of 15-deoxy-Δ12,14-prostaglandin J2 and its application in human plasma samples of patients with diabetes. Anal Bioanal Chem. 2018 Jan;410(2):521-528. doi: 10.1007/s00216-017-0748-1. Epub 2017 Nov 16.

*

Magnolol inhibits venous remodeling in mice. Sci Rep. 2017 Dec 19;7(1):17820. doi: 10.1038/s41598-017-17910-0.

*

Hypertension-evoked RhoA activity in vascular smooth muscle cells requires RGS5. FASEB J. 2017 Dec 5. pii: fj.201700384RR. doi: 10.1096/fj.201700384RR. [Epub ahead of print]

*

Role of protein carbonylation in diabetes. J Inherit Metab Dis. 2017 Nov 6. doi: 10.1007/s10545-017-0104-9. [Epub ahead of print]

*

AP-1 Oligodeoxynucleotides Reduce Aortic Elastolysis in a Murine Model of Marfan Syndrome. Mol Ther Nucleic Acids. 2017 Dec 15;9:69-79. doi: 10.1016/j.omtn.2017.08.014. Epub 2017 Sep 20.

*

Allosteric inhibition of carnosinase (CN1) by inducing a conformational shift. J Enzyme Inhib Med Chem. 2017 Dec;32(1):1102-1110. doi: 10.1080/14756366.2017.1355793.

*

Transcription factor decoy technology: a therapeutic update. Biochem Pharmacol. 2017 Nov 15;144:29-34. doi: 10.1016/j.bcp.2017.06.122. Epub 2017 Jun 19. Review.

*

Local oxygen homeostasis during various neuronal network activity states in the mouse hippocampus. J Cereb Blood Flow Metab. 2017 Nov 3; 271678X17740091. doi: 10.1177/0271678X17740091


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