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Lipopolysaccharide and Interleukin‐1β Augmented Histidine Decarboxylase Activity in Cultured Cells of the Rat Embryonic Brain
Author(s) -
Niimi Mitsuhiro,
Yamamoto Yumiko,
Takemori Hiroshi,
Uno Atsuhiko,
Kondo Yuki,
Yamatodani Atsushi
Publication year - 1997
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1997.69020851.x
Subject(s) - histidine decarboxylase , diencephalon , lipopolysaccharide , biology , cell culture , tumor necrosis factor alpha , microbiology and biotechnology , cerebral cortex , endocrinology , medicine , central nervous system , biochemistry , histidine , enzyme , genetics
We investigated the effect of lipopolysaccharide (LPS) and various inflammatory cytokines on the histidine decarboxylase (HDC) activity in cultured cells of the rat embryonic brain. Histaminergic neuronal cell bodies were supposed to exist in cultured cells of the diencephalon but not in those of the cortex. The HDC activity was elevated by adding LPS and interleukin‐1 β (IL‐1β) but not by tumor necrosis factor‐α (TNF‐α) and IL‐6 to the mixed primary cultures of diencephalon. In the adherent cell fraction of the cultured diencephalon cells, HDC activity was also enhanced by LPS and IL‐1β. In a similar manner, LPS augmented HDC activity in the mixed primary culture of cerebral cortical cells and in its adherent cell fraction. The effects of IL‐1β but not LPS in the mixed primary culture of diencephalon were canceled by a prior exposure to cytosine‐β‐ d ‐arabinofuranoside. The changes in HDC activity after exposure to LPS for 12 h were not accompanied by increased mRNA levels. In these cell cultures, mast cells were not detected by Alcian Blue staining. These results indicated the presence of the third type of HDC‐bearing cell besides neurons and mast cells in the brain. The increase of HDC activity by IL‐1β might be due to cell proliferation.