Acta Physiologica 2011; Volume 203, Supplement 686
Joint Congress of FEPS and Turkish Society of Physiological Sciences
GADOLINIUM INHIBITS MEMBRANE DEPOLARISATION-INDUCED CALCIUM SIGNALLING IN ISOLATED RAT TRIGEMINAL GANGLION NEURONS
Abstract number: PC080
Kelestimur1 Haluk, Baykara1 Murat, Kacar1 Emine, Ozcan2 Mete, Ayar3 Ahmet
1Department of Physiology, Faculty of Medicine, Firat University; Elazig, Turkey
2Department of Biophysics, Faculty of Medicine, Firat University; Elazig, Turkey
3Department of Physiology, Faculty of Medicine, Karadeniz Technical University; Trabzon, Turkey
Chelates of gadolinium are used to provide enhanced contrast between healthy and diseased tissue in nuclear magnetic resonance imaging of different organs. Gadolinium is known to block many types of calcium channels such as stretch-activated and voltage-gated calcium channels. Free gadolinium is highly toxic and can cause a variety of abnormalities. Therefore, it is crucially important that gadolinium should be strongly attached to a ligand to avoid its toxic effects. Nevertheless, some chelates of gadolinium can release gadolinium ion, and they can bring about a wide variety of changes in physiology. In this study, the effects of gadolinium on intracellular calcium concentration were investigated in isolated rat trigeminal neurons.
Trigeminal ganglion neurons were loaded with 1 mmol Fura-2 AM and calcium responses were assessed by using the fluorescent ratiometry (excitation at 340 and 380 nm, and emission at 510 nm). All data were analyzed by using an unpaired t test, with a 2-tailed P level of <0.05 defining statistical significance.
Gadolinium caused significant (P<0.001) reductions in KCL-induced increase in intracellular calcium concentration. In the presence of gadolinium, intracellular calcium increase evoked by KCL was reduced to 86.6±4.1% (n=11).
These results indicate that gadolinium can inhibit increase in intracellular calcium concentration in these sensory neurons, which might result in side effects in trigeminal functions.
To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 203, Supplement 686 :PC080