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Calcium Signalling in Mouse Bergmann Glial Cells Mediated by α 1 ‐adrenoreceptors and H 1 Histamine ‐ Receptors
Author(s) -
Kirischuk Sergej,
Tuschick Sebastian,
Verkhratsky Alexej,
Kettenmann Helmut
Publication year - 1996
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1996.tb01288.x
Subject(s) - calcium , histamine , receptor , calcium signaling , signalling , histamine receptor , neuroscience , chemistry , microbiology and biotechnology , biophysics , biology , endocrinology , biochemistry , antagonist , organic chemistry
The presence of adrenergic and histaminergic receptors in Bergmann glial cells from cerebellar slices from mice aged 20–25 days was determined using fura‐2 Ca 2+ microfluorimetry. To measure the cytoplasmic concentration of Ca 2+ ([Ca 2+ ] i ), either individual cells were loaded with the Ca 2+ ‐sensitive probe fura‐2 using the whole‐cell patch‐clamp technique or slices were incubated with a membrane‐permeable form of the dye (fura‐2/AM) and the microfluorimetric system was focused on individual cells. The monoamines adrenalin and noradrenalin (0.1‐10 μM) and histamine (10‐100 μM) triggered a transient increase in [Ca 2+ ] i . The involvement of the α 1 ‐adrenoreceptor was inferred from the observations that monoamine‐triggered [Ca 2+ ] i responses were blocked by the selective α 1 ‐adreno‐antagonist prazosin and were mimicked by the α 1 ‐adreno‐agonist phenylephrine. The monoamine‐induced [Ca 2+ ] i signals were not affected by β‐ and α 2 ‐adrenoreceptor antagonists (propranolol and yohimbine), and were not mimicked by β‐ and α 2 ‐adrenoreceptor agonists (isoproterenol and clonidine). Histamine‐induced [Ca 2+ ] i responses demonstrated specific sensitivity to only H 1 histamine receptor modulators. [Ca 2+ ] i responses to monoamines and histamine did not require the presence of extracellular Ca 2+ and they were blocked by preincubation of slices with thapsigargin (500 nM), indicating that the [Ca 2+ ] i increase is due to release from intracellular pools. No [Ca 2+ ] i responses were recorded after application of aspartate, bradykinin, dopamine, GABA, glycine, oxytocin, serotonin, somatostatin, substance P, taurine or vasopressin. We conclude that cerebellar Bergmann glial cells are endowed with α 1 ‐adrenoreceptors and H 1 histamine receptors which induce the generation of intracellular [Ca 2+ ] i signals via activation of Ca 2+ release from inositol‐l,4,5‐trisphosphate‐sensitive intracellular stores.