Effects of the histaminergic system on the morphine-induced conditioned place preference in mice

The effects of an H 2 receptor antagonist, a histidine decarboxylase inhibitor and a histamine precursor on the morphine-induced place preference in mice were examined. Morphine (1–7 mg/kg) produced a place preference in a dose-dependent manner. This morphine-induced place preference was significant...

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Veröffentlicht in:Brain research 1995-03, Vol.675 (1), p.195-202
Hauptverfasser: Suzuki, Tsutomu, Takamori, Kazuaki, Misawa, Miwa, Onodera, Kenji
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Takamori, Kazuaki
Misawa, Miwa
Onodera, Kenji
description The effects of an H 2 receptor antagonist, a histidine decarboxylase inhibitor and a histamine precursor on the morphine-induced place preference in mice were examined. Morphine (1–7 mg/kg) produced a place preference in a dose-dependent manner. This morphine-induced place preference was significantly antagonized by the dopamine (DA) D 1 receptor antagonist SCH 23390. The histamine precursor, L-histidine, attenuated the morphine (7 mg/kg)-induced place preference. On the other hand, the histidine decarboxylase inhibitor, α-fluoromethylhistidine (α-FMH), significantly potentiated the morphine (1 mg/kg)-induced place preference. This potentiation was antagonized by SCH 23390. The H 2 receptor antagonist zolantidine (0.3 mg/kg) significantly potentiated the morphine-induced place preference. Surprisingly, zolantidine (1 mg/kg) alone also produced a significant place preference. The zolantidine-induced place preference was antagonized by SCH 23390. In addition, zolantidine (1, 3 and 10 mg/kg) significantly increased DA turnover (DA ratio) in the limbic forebrain (nucleus accumbens and olfactory tubercle), implying that zolantidine may activate the mesolimbic DA system. Moreover, co-administration of zolantidine dose-dependently increased morphine (10 mg/kg)-induced DA turnover in the limbic forebrain. These results suggest that the activation of histaminergic neurons may attenuate the rewarding effect of morphine, while the inhibition of histaminergic neurons may potentiate the rewarding effect of morphine. Furthermore, potentiation of the morphine-induced rewarding effect by inhibition of histaminergic neurons may be mediated by D 1 receptors. We also demonstrated that the H 2 receptor antagonist zolantidine may activate the mesolimbic DA system, and as a result, zolantidine itself produces a rewarding effect and potentiates the morphine-induced rewarding effect.
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Morphine (1–7 mg/kg) produced a place preference in a dose-dependent manner. This morphine-induced place preference was significantly antagonized by the dopamine (DA) D 1 receptor antagonist SCH 23390. The histamine precursor, L-histidine, attenuated the morphine (7 mg/kg)-induced place preference. On the other hand, the histidine decarboxylase inhibitor, α-fluoromethylhistidine (α-FMH), significantly potentiated the morphine (1 mg/kg)-induced place preference. This potentiation was antagonized by SCH 23390. The H 2 receptor antagonist zolantidine (0.3 mg/kg) significantly potentiated the morphine-induced place preference. Surprisingly, zolantidine (1 mg/kg) alone also produced a significant place preference. The zolantidine-induced place preference was antagonized by SCH 23390. In addition, zolantidine (1, 3 and 10 mg/kg) significantly increased DA turnover (DA ratio) in the limbic forebrain (nucleus accumbens and olfactory tubercle), implying that zolantidine may activate the mesolimbic DA system. Moreover, co-administration of zolantidine dose-dependently increased morphine (10 mg/kg)-induced DA turnover in the limbic forebrain. These results suggest that the activation of histaminergic neurons may attenuate the rewarding effect of morphine, while the inhibition of histaminergic neurons may potentiate the rewarding effect of morphine. Furthermore, potentiation of the morphine-induced rewarding effect by inhibition of histaminergic neurons may be mediated by D 1 receptors. 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Morphine (1–7 mg/kg) produced a place preference in a dose-dependent manner. This morphine-induced place preference was significantly antagonized by the dopamine (DA) D 1 receptor antagonist SCH 23390. The histamine precursor, L-histidine, attenuated the morphine (7 mg/kg)-induced place preference. On the other hand, the histidine decarboxylase inhibitor, α-fluoromethylhistidine (α-FMH), significantly potentiated the morphine (1 mg/kg)-induced place preference. This potentiation was antagonized by SCH 23390. The H 2 receptor antagonist zolantidine (0.3 mg/kg) significantly potentiated the morphine-induced place preference. Surprisingly, zolantidine (1 mg/kg) alone also produced a significant place preference. The zolantidine-induced place preference was antagonized by SCH 23390. In addition, zolantidine (1, 3 and 10 mg/kg) significantly increased DA turnover (DA ratio) in the limbic forebrain (nucleus accumbens and olfactory tubercle), implying that zolantidine may activate the mesolimbic DA system. Moreover, co-administration of zolantidine dose-dependently increased morphine (10 mg/kg)-induced DA turnover in the limbic forebrain. These results suggest that the activation of histaminergic neurons may attenuate the rewarding effect of morphine, while the inhibition of histaminergic neurons may potentiate the rewarding effect of morphine. Furthermore, potentiation of the morphine-induced rewarding effect by inhibition of histaminergic neurons may be mediated by D 1 receptors. 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Psychology</topic><topic>Histamine - physiology</topic><topic>Histamine H2 Antagonists - pharmacology</topic><topic>Histidine - pharmacology</topic><topic>Histidine Decarboxylase - antagonists &amp; inhibitors</topic><topic>Homovanillic Acid - metabolism</topic><topic>l-Histidine</topic><topic>Limbic System - drug effects</topic><topic>Limbic System - metabolism</topic><topic>Male</topic><topic>Methylhistidines - pharmacology</topic><topic>Mice</topic><topic>Mice, Inbred Strains</topic><topic>Morphine</topic><topic>Morphine - pharmacology</topic><topic>Neurotransmission and behavior</topic><topic>Phenoxypropanolamines</topic><topic>Piperidines - pharmacology</topic><topic>Prosencephalon - drug effects</topic><topic>Prosencephalon - metabolism</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychology. Psychophysiology</topic><topic>SCH 23390</topic><topic>Thiazoles - pharmacology</topic><topic>Zolantidine</topic><topic>α-Fluoromethylhistidine (α-FMH)</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Suzuki, Tsutomu</creatorcontrib><creatorcontrib>Takamori, Kazuaki</creatorcontrib><creatorcontrib>Misawa, Miwa</creatorcontrib><creatorcontrib>Onodera, Kenji</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Suzuki, Tsutomu</au><au>Takamori, Kazuaki</au><au>Misawa, Miwa</au><au>Onodera, Kenji</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of the histaminergic system on the morphine-induced conditioned place preference in mice</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>1995-03-27</date><risdate>1995</risdate><volume>675</volume><issue>1</issue><spage>195</spage><epage>202</epage><pages>195-202</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>The effects of an H 2 receptor antagonist, a histidine decarboxylase inhibitor and a histamine precursor on the morphine-induced place preference in mice were examined. Morphine (1–7 mg/kg) produced a place preference in a dose-dependent manner. This morphine-induced place preference was significantly antagonized by the dopamine (DA) D 1 receptor antagonist SCH 23390. The histamine precursor, L-histidine, attenuated the morphine (7 mg/kg)-induced place preference. On the other hand, the histidine decarboxylase inhibitor, α-fluoromethylhistidine (α-FMH), significantly potentiated the morphine (1 mg/kg)-induced place preference. This potentiation was antagonized by SCH 23390. The H 2 receptor antagonist zolantidine (0.3 mg/kg) significantly potentiated the morphine-induced place preference. Surprisingly, zolantidine (1 mg/kg) alone also produced a significant place preference. The zolantidine-induced place preference was antagonized by SCH 23390. In addition, zolantidine (1, 3 and 10 mg/kg) significantly increased DA turnover (DA ratio) in the limbic forebrain (nucleus accumbens and olfactory tubercle), implying that zolantidine may activate the mesolimbic DA system. Moreover, co-administration of zolantidine dose-dependently increased morphine (10 mg/kg)-induced DA turnover in the limbic forebrain. These results suggest that the activation of histaminergic neurons may attenuate the rewarding effect of morphine, while the inhibition of histaminergic neurons may potentiate the rewarding effect of morphine. Furthermore, potentiation of the morphine-induced rewarding effect by inhibition of histaminergic neurons may be mediated by D 1 receptors. We also demonstrated that the H 2 receptor antagonist zolantidine may activate the mesolimbic DA system, and as a result, zolantidine itself produces a rewarding effect and potentiates the morphine-induced rewarding effect.</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>7796129</pmid><doi>10.1016/0006-8993(95)00064-W</doi><tpages>8</tpages></addata></record>
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ispartof Brain research, 1995-03, Vol.675 (1), p.195-202
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source MEDLINE; Elsevier ScienceDirect Journals
subjects 3,4-Dihydroxyphenylacetic Acid - metabolism
Animals
Behavioral psychophysiology
Benzazepines - pharmacology
Benzothiazoles
Biological and medical sciences
Conditioned place preference
Conditioning, Operant - drug effects
DA turnover
Dihydroxyphenylalanine - metabolism
Dopamine - metabolism
Dose-Response Relationship, Drug
Fundamental and applied biological sciences. Psychology
Histamine - physiology
Histamine H2 Antagonists - pharmacology
Histidine - pharmacology
Histidine Decarboxylase - antagonists & inhibitors
Homovanillic Acid - metabolism
l-Histidine
Limbic System - drug effects
Limbic System - metabolism
Male
Methylhistidines - pharmacology
Mice
Mice, Inbred Strains
Morphine
Morphine - pharmacology
Neurotransmission and behavior
Phenoxypropanolamines
Piperidines - pharmacology
Prosencephalon - drug effects
Prosencephalon - metabolism
Psychology. Psychoanalysis. Psychiatry
Psychology. Psychophysiology
SCH 23390
Thiazoles - pharmacology
Zolantidine
α-Fluoromethylhistidine (α-FMH)
title Effects of the histaminergic system on the morphine-induced conditioned place preference in mice
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