The 5-HT5A serotonin receptor is expressed predominantly by astrocytes in which it inhibits cAMP accumulation: A mechanism for neuronal suppression of reactive astrocytes
Monica J. Carson
Department of Molecular Biology, The Scripps Research Institute, La Jolla, California 92037
Search for more papers by this authorElizabeth A. Thomas
Department of Molecular Biology, The Scripps Research Institute, La Jolla, California 92037
Search for more papers by this authorPatria E. Danielson
Department of Molecular Biology, The Scripps Research Institute, La Jolla, California 92037
Search for more papers by this authorCorresponding Author
J. Gregor Sutcliffe
Department of Molecular Biology, The Scripps Research Institute, La Jolla, California 92037
Dept. of Molecular Biology, The Scripps Research Institute, 10666 North Torrey Pines Rd., La Jolla, CA 92037Search for more papers by this authorMonica J. Carson
Department of Molecular Biology, The Scripps Research Institute, La Jolla, California 92037
Search for more papers by this authorElizabeth A. Thomas
Department of Molecular Biology, The Scripps Research Institute, La Jolla, California 92037
Search for more papers by this authorPatria E. Danielson
Department of Molecular Biology, The Scripps Research Institute, La Jolla, California 92037
Search for more papers by this authorCorresponding Author
J. Gregor Sutcliffe
Department of Molecular Biology, The Scripps Research Institute, La Jolla, California 92037
Dept. of Molecular Biology, The Scripps Research Institute, 10666 North Torrey Pines Rd., La Jolla, CA 92037Search for more papers by this authorAbstract
The mRNA for the 5-hydroxytryptamine receptor 5-HT5A was detected at embryonic day 18 in the rat central nervous system and peaked by postnatal day 20. At all time points examined, 5-HT5A immunoreactivity observed on astrocyte cell bodies and in the stellate processes not only colocalized with the astrocyte-specific marker glial fibrillary acidic protein (GFAP) but was coordinately regulated with GFAP, increasing during development and during gliosis. Transfection of 5-HT5A into glioma cells prevented the 5-HT-induced increase in cAMP observed in untransfected cells and decreased the relative forskolin response by approximately 20%, suggesting that the 5-HT5A receptor couples negatively to adenylyl cyclase in astrocytes. Together, these results indicate a neuron-to-astrocyte serotonergic signaling pathway mediating cAMP concentrations, which could provide a neuronally driven mechanism for regulating astrocyte physiology with relevance to gliosis. © 1996 Wiley-Liss, Inc.
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