Biologia, Bratislava 54/Suppl. 6: 109-114, 1999.

ISSN 0006-3088 (Biologia). ISSN 1335-6399 (Biologia. Section Cellular and Molecular Biology).


Full paper

The inositol (1,4,5) trisphosphate receptors and calreticulin in calcium stores from the gerbil forebrain after global ischemia-reperfusion injury.


Jan Lehotsky1*, Peter Racay1, Peter Kaplan1, Radovan Murin1, Milena Matejovicova1, Luc Raeymaekers2 & Viera Mezesova1

1 Department of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius University, Mala Hora 4, SK-03601 Martin, Slovakia; tel.: 421 842 31565, fax: 421 842 36770, e-mail:

2 Laboratory for Physiology, Catholic University Leuven, Campus Gasthuisberg, B-3000 Leuven, Belgium

* corresponding author

Received: December 16, 1998 / Accepted: October 5, 1999



Using immunological method we have identified the proteins of the intracellular Ca2+ release mechanism in the gerbil forebrain: InsP3 receptor type I and intra-organellar Ca2+ binding protein calreticulin. The antibodies to InsP3 receptor type II gave no positive signal in the forebrain. The results of quantitative Western blotting indicate a selective alteration of InsP3 receptor type I protein level but no changes in intraluminal calreticulin after a global forebrain ischemia followed by a prolonged reperfusion period. We suppose that a selective alteration of Ca2+ handling proteins observed during the recirculation period, may contribute to the changes which lead to the derangement of Ca2+ homeostasis in neuronal cells and may participate and/or follow the neuronal death in gerbils.


Key words: gerbil forebrain, calcium stores, inositol (1,4,5) trisphosphate receptor, calreticulin.