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Effects of prostaglandin E 2 and cyclooxygenase inhibitors on clustering and level of nicotinic acetylcholine receptor in mouse myotubes co‐cultured with spinal cord explant
Author(s) -
Kimura I.,
Nakagawa M.,
Kobayashi S.,
Kimura M.
Publication year - 1991
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/0736-5748(91)90057-s
Subject(s) - acetylcholine receptor , nicotinic agonist , myogenesis , nicotinic acetylcholine receptor , explant culture , ganglion type nicotinic receptor , chemistry , acetylcholine , spinal cord , cyclooxygenase , pharmacology , prostaglandin e2 , microbiology and biotechnology , biology , receptor , neuroscience , endocrinology , biochemistry , myocyte , enzyme , in vitro
The clustering and level of nicotinic acetylcholine receptor (n‐AChR) in cultured mouse myotubes are negatively controlled by endogenous phospholipase A 2 (PLA 2 ) (Kimura et al., Int. J. Devl. Neurosci. 5 , 127–133, 1987). The effects of PLA 2 ‐related metabolites, prostaglandins, leukotrienes and platelet‐activating factor (PAF) were investigated using fluorescein isothiocyanate‐α‐bungarotoxin. Peak and total fluorescence within a cluster were used as indices of clustering and level of n‐AChR, respectively. Prostaglandin E 2 (PGE 2 , 1–10 μm) decreased both indices in a concentration‐dependent manner. Aspirin and indomethacin, cyclooxygenase inhibitors, increased the indices at 1.0 μM and 10–30 nM, and decreased them at higher concentrations of 10–30 μM and 0.1–1 μM, respectively. Prostaglandin F 2α (PGF 2α , 1–10 μM), nordihydroguaiaretic acid (30 μM), a lipoxygenase inhibitor, and PAF (10 μM) had no effect. These results suggest that the control of endogenous PLA 2 on the clustering and level of n‐AChR is due to PGE 2 , but not to PGF 2α , leukotrienes or PAF.