Background: Enteric glial cells show morphological similarities to astrocytes, but little is known about their regulation. Methods: The effects 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 stained positive for glutamine synthetase, S-100, and glial fibrillary acidic protein, and rapid elevations of intracellular Ca2+ were observed in response to endothelin-1, extracellular adenosine 5’-triphosphate, uridine 5’-triphosphate, and vasopressin. In enteroglia, endothelin-1 induced a calcium signal different from that evoked in astrocytes. In contrast to astrocytes, enteroglia did not show an increase of intracellular Ca2+ following addition of angiotensin II, bradykinin, α-adrenergic agonists, carbachol, prostaglandin E2, glutamate, dopamine, epidermal growth factor, substance P, or neurokinins, and only 5-15% of the enteroglial cells responded to serotonin, histamine, epinephrine, and prostaglandin F2α. Hypoosmotic exposure led to a rapid increase of intracellular Ca2+ concentration followed by a sustained plateau in astrocytes. In enteroglia, hypoosmolarity did not evoke an initial Ca2+ spike, but led to a slow increase of intracellular Ca2+, due to influx from the extracellular space. Conclusion: There are marked differences between enteroglia and brain astrocytes with respect to their regulation by calcium-mobilizing agonists and hypoosmolarity.

Journal Section:
Original Paper
Keywords:
Enteroglia, Astrocytes, Calcium, Endothelin-1, Vasopressin, Hypoosmolarity, Nucleotides
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© 1997 S. Karger AG, Basel
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1997
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