Abstract

Mechanisms underlying intracellular calcium signals in Bergmann glial cells evoked by various neurotransmitters were investigated in experiments on cerebellar slices acutely isolated from 30-day-old mice. [Ca2+] in values were measured by means of a Ca2+-sensitive fluorescent probe fura-2. Extracellular application of ATP (10–100 µM), histamine (10–100 µM), or noradrenaline (or adrenaline, 0.1–10.0 µM) caused a temporary increase in cytoplasmic Ca2+ concentrations. The effect persisted in Ca2+-free extracellular solution and was blocked with thapsigargin (500 nM) or a specific blocker of the inositol-1,4,5-trisphosphate-sensitive intracellular channels heparin. Based on the pharmacological analysis, we postulate the involvement of P2 purinoreceptors, α1-adrenoreceptors, and H1 histamine receptors in an agonist-activated increase in [Ca2+] in in Bergmann glia. Thus, ATP, monoamines, or histamine induce calcium signal generation in Bergmann glial cells via activation of Ca2+ release from the inositol-1,4,5-trisphosphate-sensitive internal stores.

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