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Effects of adenylyl cyclase‐linked neuropeptides on the expression of ciliary neurotrophic factor‐mRNA in cultured astrocytes
Author(s) -
Nagao Hiroshi,
Matsuoka Ichiro,
Kurihara Kenzo
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00214-t
Subject(s) - ciliary neurotrophic factor , forskolin , cycloheximide , adenylyl cyclase , medicine , olfactory bulb , endocrinology , biology , messenger rna , neurotrophic factors , microbiology and biotechnology , chemistry , central nervous system , protein biosynthesis , stimulation , biochemistry , receptor , gene
Ciliary neurotrophic factor (CNTF) is a molecule which has profound effects on various neural cell types. In the central nervous system, expression of CNTF‐mRNA is highly concentrated in olfactory bulb. In the present study, we examined the regulatory mechanism of CNTF‐mRNA expression in cultured astrocytes from newborn rat brain. Cultured astrocytes from new born rat brain expressed CNTF‐mRNA at levels comparable to the level in olfactory bulb in vivo. Treatment of the astrocytes with forskolin, an activator of adenylyl cyclase, led to a decrease of CNTF‐mRNA level. The effect of forskolin was mimicked by cAMP‐linked agonists, such as VIP, PACAP, isoproterenol and dopamine. Cycloheximide, an inhibitor of protein synthesis, did not abolish the forskolin‐induced decrease of CNTF‐mRNA. Measurement of the half‐life of CNTF‐mRNA in the presence of actinomycin D, an inhibitor of transcription, indicated that the degradation of CNTF‐mRNA is not destabilized by the forskolin‐treatment. These data taken together suggest that the cAMP‐induced suppression of CNTF‐mRNA is mainly caused by the inhibition of CNTF gene transcription.