Histamine H<inf>2</inf>-receptor mediated activation of neonatal rat brain ornithine decarboxylase in vivo

Jose Rodriguez; Alfonso Toledo; Regina Brandner; Ricardo Rodriguez; Josefa Sabria; Isaac Blanco

doi:https://doi.org/10.1016/0006-2952(88)90228-6

Histamine H<inf>2</inf>-receptor mediated activation of neonatal rat brain ornithine decarboxylase in vivo

Jose Rodriguez, Alfonso Toledo, Regina Brandner, Ricardo Rodriguez, Josefa Sabria, Isaac Blanco

Department of Biochemistry and Molecular Biology

Research output: Contribution to journal › Article › Research › peer-review

8 Citations (Scopus)

Abstract

The effect of histamine (HA) administered via intracerebroventricular injection on ornithine decarboxylase (ODC) activity was studied in neonatal rat brain. The HA effect was dose and time dependent. Maximal increase in ODC activity was achieved 2 hr after administration of 10 μg HA (38% over control levels). Impromidine (HA H2-agonist) mimicked the effect of HA on ODC and ranitidine (HA H2-antagonist) inhibited the response to HA. Neither 2-thiazolylethylamine (HA H1-agonist) nor mepyramine (HA H1-antagonist) modified control ODC activity. The HA-releasers, compound 48/80 and polymixin B sulfate, elicited an increase in brain ODC activity of 35% and 32%, respectively, over the control value. © 1988.

Original language	English
Pages (from-to)	551-554
Journal	Biochemical Pharmacology
Volume	37
DOIs	https://doi.org/10.1016/0006-2952(88)90228-6
Publication status	Published - 1 Feb 1988

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title = "Histamine H2-receptor mediated activation of neonatal rat brain ornithine decarboxylase in vivo",

abstract = "The effect of histamine (HA) administered via intracerebroventricular injection on ornithine decarboxylase (ODC) activity was studied in neonatal rat brain. The HA effect was dose and time dependent. Maximal increase in ODC activity was achieved 2 hr after administration of 10 μg HA (38% over control levels). Impromidine (HA H2-agonist) mimicked the effect of HA on ODC and ranitidine (HA H2-antagonist) inhibited the response to HA. Neither 2-thiazolylethylamine (HA H1-agonist) nor mepyramine (HA H1-antagonist) modified control ODC activity. The HA-releasers, compound 48/80 and polymixin B sulfate, elicited an increase in brain ODC activity of 35% and 32%, respectively, over the control value. {\textcopyright} 1988.",

author = "Jose Rodriguez and Alfonso Toledo and Regina Brandner and Ricardo Rodriguez and Josefa Sabria and Isaac Blanco",

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T1 - Histamine H2-receptor mediated activation of neonatal rat brain ornithine decarboxylase in vivo

AU - Rodriguez, Jose

AU - Toledo, Alfonso

AU - Brandner, Regina

AU - Rodriguez, Ricardo

AU - Sabria, Josefa

AU - Blanco, Isaac

PY - 1988/2/1

Y1 - 1988/2/1

N2 - The effect of histamine (HA) administered via intracerebroventricular injection on ornithine decarboxylase (ODC) activity was studied in neonatal rat brain. The HA effect was dose and time dependent. Maximal increase in ODC activity was achieved 2 hr after administration of 10 μg HA (38% over control levels). Impromidine (HA H2-agonist) mimicked the effect of HA on ODC and ranitidine (HA H2-antagonist) inhibited the response to HA. Neither 2-thiazolylethylamine (HA H1-agonist) nor mepyramine (HA H1-antagonist) modified control ODC activity. The HA-releasers, compound 48/80 and polymixin B sulfate, elicited an increase in brain ODC activity of 35% and 32%, respectively, over the control value. © 1988.

AB - The effect of histamine (HA) administered via intracerebroventricular injection on ornithine decarboxylase (ODC) activity was studied in neonatal rat brain. The HA effect was dose and time dependent. Maximal increase in ODC activity was achieved 2 hr after administration of 10 μg HA (38% over control levels). Impromidine (HA H2-agonist) mimicked the effect of HA on ODC and ranitidine (HA H2-antagonist) inhibited the response to HA. Neither 2-thiazolylethylamine (HA H1-agonist) nor mepyramine (HA H1-antagonist) modified control ODC activity. The HA-releasers, compound 48/80 and polymixin B sulfate, elicited an increase in brain ODC activity of 35% and 32%, respectively, over the control value. © 1988.

U2 - https://doi.org/10.1016/0006-2952(88)90228-6

DO - https://doi.org/10.1016/0006-2952(88)90228-6

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