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The 5‐HT 5A serotonin receptor is expressed predominantly by astrocytes in which it inhibits cAMP accumulation: A mechanism for neuronal suppression of reactive astrocytes
Author(s) -
Carson Monica J.,
Thomas Elizabeth A.,
Danielson Patria E.,
Sutcliffe J. Gregor
Publication year - 1996
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/(sici)1098-1136(199608)17:4<317::aid-glia6>3.0.co;2-w
Subject(s) - astrocyte , biology , glial fibrillary acidic protein , gliosis , serotonergic , neuroglia , receptor , microbiology and biotechnology , neuron , serotonin , 5 ht receptor , adenylyl cyclase , medicine , forskolin , neuroscience , endocrinology , signal transduction , central nervous system , immunology , genetics , immunohistochemistry
The mRNA for the 5‐hydroxytryptamine receptor 5‐HT 5A was detected at embryonic day 18 in the rat central nervous system and peaked by postnatal day 20. At all time points examined, 5‐HT 5A 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‐HT 5A 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‐HT 5A 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.