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IN VIVO FORMATION AND CATABOLISM OF [ 14 C]HISTAMINE IN MOUSE BRAIN
Author(s) -
Schayer R. W.,
Reilly Margaret A.
Publication year - 1970
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.1471-4159.1970.tb11389.x
Subject(s) - histamine , catabolism , histamine n methyltransferase , histidine , diamine oxidase , histidine decarboxylase , chemistry , decarboxylation , in vivo , monoamine oxidase , biochemistry , metabolism , endocrinology , medicine , biology , histamine h2 receptor , amino acid , enzyme , receptor , catalysis , microbiology and biotechnology , antagonist
— The formation of histamine in brain was studied in mice injected with l ‐[ 14 C]‐histidine (ring 2‐ 14 C) intravenously (i.v.) or intracerebrally; [ 14 C]histamine appeared rapidly and exhibited a rapid rate of turnover. Drugs known to block various pathways of histamine catabolism were tested for effects on brain–[ 14 C]histamine and [ 14 C]‐methyl‐histamine in mice given (1) [ 14 C]histamine i.v., (2) [ 14 C]histamine intracerebrally, and (3) l ‐[ 14 C]histidine i.v. Blood‐borne histamine did not enter brain; brain histamine was formed locally by decarboxylation of histidine Methylhistamine did cross the blood‐brain barrier. Methylation was the major route of histamine catabolism in mouse brain and some of the methylhistamine formed was destroyed by monoamine oxidase. No evidence for catabolism by the action of diamine oxidase was found.