S. Kirischuk et al., CALCIUM SIGNALING IN MOUSE BERGMANN GLIAL-CELLS MEDIATED BY ALPHA(1)-ADRENOCEPTORS AND H-1 HISTAMINE-RECEPTORS, European journal of neuroscience, 8(6), 1996, pp. 1198-1208
The presence of adrenergic and histaminergic receptors in Bergmann gli
al cells from cerebellar slices from mice aged 20-25 days was determin
ed using fura-2 Ca2+ microfluorimetry. To measure the cytoplasmic conc
entration of Ca2+ ([Ca2+](i)), either individual cells were loaded wit
h the Ca2+-sensitive probe fura-2 using the whole-cell patch-clamp tec
hnique or slices were incubated with a membrane-permeable form of the
dye (fura-2/AM) and the microfluorimetric system was focused on indivi
dual cells. The monoamines adrenalin and noradrenalin (0.1-10 mu M) an
d histamine (10-100 mu M) triggered a transient increase in [Ca2+](i).
The involvement of the alpha(1)-adrenoreceptor was inferred from the
observations that monoamine-triggered [Ca2+](i) responses were blocked
by the selective alpha(1)-adreno-antagonist prazosin and were mimicke
d by the alpha(1)-adreno-agonist phenylephrine. The monoamine-induced
[Ca2+](i) signals were not affected by beta- and alpha(2)-adrenorecept
or antagonists (propranolol and yohimbine), and were not mimicked by b
eta- and alpha(2)-adrenoreceptor agonists (isoproterenol and clonidine
). Histamine-induced [Ca2+](i) responses demonstrated specific sensiti
vity to only H-1 histamine receptor modulators. [Ca2+](i) responses to
monoamines and histamine did not require the presence of extracellula
r Ca2+ and they were blocked by preincubation of slices with thapsigar
gin (500 nM), indicating that the [Ca2+](i) increase is due to release
from intracellular pools. No [Ca2+](i) responses were recorded after
application of aspartate, bradykinin, dopamine, GABA, glycine, oxytoci
n, serotonin, somatostatin, substance P, taurine or vasopressin. We co
nclude that cerebellar Bergmann glial cells are endowed with alpha(1)-
adrenoreceptors and H-1 histamine receptors which induce the generatio
n of intracellular [Ca2+](i) signals via activation of Ca2+ release fr
om inositol-1,4,5-trisphosphate-sensitive intracellular stores.