Regionally Distinct Regulation of Astroglial Neurotransmitter Receptors by Fibroblast Growth Factor-2

• Published in: Molecular and cellular neuroscience 2000-07, Vol.16 (1), p.42-58
• Main Authors: Reuss, Bernhard, Leung, Doreen S.Y., Ohlemeyer, Carsten, Kettenmann, Helmut, Unsicker, Klaus
• Format: Article
• Language: English
• Subjects: Animals; Animals, Newborn; Astrocytes - cytology; Astrocytes - drug effects; Astrocytes - metabolism; Calcium - metabolism; Cell Count - drug effects; Cells, Cultured; Cerebral Cortex - cytology; Cerebral Cortex - drug effects; Cerebral Cortex - metabolism; Corpus Striatum - cytology; Corpus Striatum - drug effects; Corpus Striatum - metabolism; Dopamine - metabolism; Dopamine - pharmacology; Dopamine Agonists - pharmacology; Fibroblast Growth Factor 2 - metabolism; Fibroblast Growth Factor 2 - pharmacology; Gap Junctions - drug effects; Gap Junctions - metabolism; Glutamic Acid - metabolism; Glutamic Acid - pharmacology; Glycyrrhetinic Acid - analogs & derivatives; Glycyrrhetinic Acid - pharmacology; Intracellular Fluid - drug effects; Intracellular Fluid - metabolism; Mesencephalon - cytology; Mesencephalon - drug effects; Mesencephalon - metabolism; Octanols - pharmacology; Rats; Receptors, Dopamine D1 - agonists; Receptors, Dopamine D1 - biosynthesis; Receptors, Dopamine D1 - genetics; Receptors, Neurotransmitter - metabolism; RNA, Messenger - biosynthesis
• ISSN: 1044-7431; 1095-9327
• DOI: 10.1006/mcne.2000.0857

Fibroblast growth factor (FGF)-2 is an abundant astroglial cytokine. We have previously shown that FGF-2 downregulates gap junctions in primary astroglial cultures (B. Reuss et al., 1998, Glia 22, 19–30). We demonstrate now that FGF-2 induces astroglial dopamine (DA) sensitivity and D1 dopamine-receptor (D1DR) antigen and message in cortical and striatal astroglial cultures. On the functional level 10 μmol/L DA triggered transient increases in astroglial [Ca2+]i. In gap-junction-coupled cells, no FGF-2-dependent changes in proportions of DA-responsive cells were observable. However, uncoupling with octanol or 18α-glycirrhetinic acid isolated the smaller population of astrocytes intrinsically sensitive to DA which was significantly increased by FGF-2 in cortical and striatal cultures. Administration of DR-specific substances revealed that FGF-2 upregulated D1DR. These results indicate that downregulation of astroglial gap junctions by FGF-2 is accompanied by an upregulation of D1DR and DA sensitivity, adding a new aspect to the role of FGF-2 in the regulation of brain functions.