The assumption that hypoxic tolerance induced by preconditioning with moderate hypobaric hypoxia (MHH) includes modifi cation of intracellular Ca2+ (Ca2+ i ) transients by modulation of glutamate receptors (GluR) activity was tested. Superfused rat brain slices were prepared 24 hours after three MHH sessions equivalent to 5 000 m above see level and tested by application of selective agonists of different subtypes of GluR. Ca2+ i level in response to the agonists was increased in comparison with the control ones. The most prominent Ca2+ level shifts were recorded in response to stimulation of group I metabotropic glutamate receptors (ImGluRs). The modifi ed pattern of the responses showed striking prevalence of signal pathways responsible for Ca2+ release from intracellular stores against modulation of Ca2+ entry. The selective antagonism of both 1 and 5 subtypes of ImGluRs in vivo during MHH did not suppress the preconditioning effi ciency, tested in the slices by severe (10 min) anoxia 24 hours after. Moreover by immunocytochemical and Western-blotting methods we found no valid distinctions in a peptide expression of these ImGluRs subtypes between control and MHHpreconditiond rats. Thus it can be supposed that the changed pattern of Ca2+ response to the agonist and mechanisms of brain tolerance induced by MHH are determined by a shift in balance of different glutamatergic signal pathways controlling the dynamics of Ca2+ i level rather than by modifi cation of the agonist reception.
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