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An Ex Vivo Method for Evaluating Prostaglandin Synthetase Activity in Cortical Slices of Mouse Brain
Author(s) -
Shohami E.,
Gross J.
Publication year - 1985
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 - 10.1111/j.1471-4159.1985.tb05484.x
Subject(s) - in vivo , prostaglandin e2 , incubation , flufenamic acid , prostaglandin , chemistry , ex vivo , in vitro , slice preparation , prostaglandin e , pharmacology , endocrinology , medicine , biochemistry , biology , microbiology and biotechnology
The release of prostaglandin E 2 (PGE 2 ) from cortical slices of mice into incubation medium is followed for 3 h and compared to PGE 2 levels in the corresponding slice. Immediately after decapitation, the rate of PGE 2 released into the incubation medium is elevated and a steady low rate of spontaneous release is gained within 1–2 h of incubation. PGE 2 synthesis and release is blocked in a dose‐dependent manner by either indometh‐acin (3 × 1(10 −6 ‐ 3 × 10 −4 M ) or flufenamic acid (2.6 × 10 −6 M ) either when added in vitro or administered in vivo. Full recovery of PGE 2 synthesis is reached after 3 h incubation of slices following in vivo administration, of indomethacin. In vivo administration of flufenamic acid results in prolonged inhibition of PGE 2 released in vitro. The inhibition of PGE 2 released by indomethacin is also correlated with the slice PGE 2 content. Administration of lipopolysaccharide (LPS), a known activator of phospho‐lipase A 2 , results in a fivefold increase in PGE 2 and a twofold increase in 6‐keto‐PGF lQ released into the medium. The release of thromboxane B 2 is not affected by LPS.