Receptor-stimulated system mediated interactions of neuropeptides in GH3 cells.
The interaction between two neuropeptides, VIP and TRH, was studied. The TRH receptor binding ability was examined using intact GH3 cells and its membrane fraction. The TRH binding ability decreased when intact cells were preincubated with VIP, forskolin or db-cAMP, but not when the membrane fraction was treated with these agents. The binding was reduced only when the membrane fraction was treated with catalytic subunit of cAMP dependent protein kinase (A-kinase). These results indicate that the binding ability of TRH receptors, which are linked to inositol phospholipid metabolism, is suppressed when A-kinase increases due to activation of the adenylate cyclase or its dependent system. This, in turn, suggests the presence of a communication via a cytoplasmic factor (probably A-kinase) between the two principal second messenger systems in the cell.
Ogawa
N
N
Institute for Neurobiology, Okayama University Medical School, Japan.
Haba
K
K
Hirakawa
S
S
Mizukawa
K
K
Tsushima
T
T
D000818:Animals; D003994:Bucladesine / Q000494:pharmacology; D002460:Cell Line; D005576:Colforsin / Q000494:pharmacology; D005910:Glioma / Q000378:metabolism*; D007700:Kinetics; D015240:Phorbol 12,13-Dibutyrate / Q000494:pharmacology; D017981:Receptors, Neurotransmitter / Q000187:drug effects / Q000378:metabolism*; D018025:Receptors, Thyrotropin-Releasing Hormone; D013973:Thyrotropin-Releasing Hormone / Q000378:metabolism*; D014660:Vasoactive Intestinal Peptide / Q000494:pharmacology
D017981:Receptors, Neurotransmitter; D018025:Receptors, Thyrotropin-Releasing Hormone; D005576:Colforsin; D014660:Vasoactive Intestinal Peptide; D015240:Phorbol 12,13-Dibutyrate; D013973:Thyrotropin-Releasing Hormone; D003994:Bucladesine