R. Fischer et al., AGONIST-INDUCED CA2-CELLS AND ASTROCYTES - A COMPARATIVE-STUDY( TRANSIENTS IN CULTURED RAT ENTERIC GLIAL), Cellular physiology and biochemistry, 7(2), 1997, pp. 93-106
Background: Enteric glial cells show morphological similarities to ast
rocytes, but little is known about their regulation. Methods: The effe
cts of various agonists on intracellular Ca2+ were studied by means of
fura-2 fluorescence at the single-cell level in cultured rat enteric
glial cells and primary rat astrocytes. Results: Both cell types stain
ed positive for glutamine synthetase, S-100, and glial fibrillary acid
ic protein, and rapid elevations of intracellular Ca2+ were observed i
n response to endothelin-1, extracellular adenosine 5'-triphosphate, u
ridine 5'-triphosphate, and vasopressin. In enteroglia, endothelin-1 i
nduced a calcium signal different from that evoked in astrocytes. In c
ontrast to astrocytes, enteroglia did not show an increase of intracel
lular Ca2+ following addition of angiotensin II, bradykinin, a-adrener
gic agonists, carbachol, prostaglandin E-2, glutamate, dopamine, epide
rmal growth factor, substance P, or neurokinins, and only 5-15% of the
enteroglial cells responded to serotonin, histamine, epinephrine, and
prostaglandin F-2 alpha. Hypoosmotic exposure led to a rapid increase
of intracellular Ca2+ concentration followed by a sustained plateau i
n astrocytes. In enteroglia, hypoosmolarity did not evoke an initial C
a2+ spike, but led to a slow increase of intracellular Ca2+, due to in
flux from the extracellular space. Conclusion: There are marked differ
ences between enteroglia and brain astrocytes with respect to their re
gulation by calcium-mobilizing agonists and hypoosmolarity.