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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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. |
doi_str_mv | 10.1016/0006-8993(95)00064-W |
format | Article |
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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.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/0006-8993(95)00064-W</identifier><identifier>PMID: 7796129</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier B.V</publisher><subject>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)</subject><ispartof>Brain research, 1995-03, Vol.675 (1), p.195-202</ispartof><rights>1995</rights><rights>1995 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c483t-b4a1051bc667df10d1d5883df870e75a215462bfa60cde26087af0a8191525dc3</citedby><cites>FETCH-LOGICAL-c483t-b4a1051bc667df10d1d5883df870e75a215462bfa60cde26087af0a8191525dc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/000689939500064W$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3466252$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7796129$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Suzuki, Tsutomu</creatorcontrib><creatorcontrib>Takamori, Kazuaki</creatorcontrib><creatorcontrib>Misawa, Miwa</creatorcontrib><creatorcontrib>Onodera, Kenji</creatorcontrib><title>Effects of the histaminergic system on the morphine-induced conditioned place preference in mice</title><title>Brain research</title><addtitle>Brain Res</addtitle><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.</description><subject>3,4-Dihydroxyphenylacetic Acid - metabolism</subject><subject>Animals</subject><subject>Behavioral psychophysiology</subject><subject>Benzazepines - pharmacology</subject><subject>Benzothiazoles</subject><subject>Biological and medical sciences</subject><subject>Conditioned place preference</subject><subject>Conditioning, Operant - drug effects</subject><subject>DA turnover</subject><subject>Dihydroxyphenylalanine - metabolism</subject><subject>Dopamine - metabolism</subject><subject>Dose-Response Relationship, Drug</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Histamine - physiology</subject><subject>Histamine H2 Antagonists - pharmacology</subject><subject>Histidine - pharmacology</subject><subject>Histidine Decarboxylase - antagonists & inhibitors</subject><subject>Homovanillic Acid - metabolism</subject><subject>l-Histidine</subject><subject>Limbic System - drug effects</subject><subject>Limbic System - metabolism</subject><subject>Male</subject><subject>Methylhistidines - pharmacology</subject><subject>Mice</subject><subject>Mice, Inbred Strains</subject><subject>Morphine</subject><subject>Morphine - pharmacology</subject><subject>Neurotransmission and behavior</subject><subject>Phenoxypropanolamines</subject><subject>Piperidines - pharmacology</subject><subject>Prosencephalon - drug effects</subject><subject>Prosencephalon - metabolism</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychology. Psychophysiology</subject><subject>SCH 23390</subject><subject>Thiazoles - pharmacology</subject><subject>Zolantidine</subject><subject>α-Fluoromethylhistidine (α-FMH)</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU-LFDEQxYMo67j6DRT6IIseWvM_6Ysgy-oKC16UPcZMUnEi3Umb9Czst9_0zjBHPaUe71dF5RVCrwn-QDCRHzHGstfDwN4N4v0qeH_7BG2IVrSXlOOnaHNCnqMXtf5pkrEBn6EzpQZJ6LBBv65CALfULodu2UG3i3WxU0xQfkfX1fu6wNTl9OhNucy7ZvUx-b0D37mcfFxiTq2eR-ugmwsEKJBaGVM3RQcv0bNgxwqvju85-vnl6sfldX_z_eu3y883veOaLf2WW4IF2ToplQ8Ee-KF1swHrTAoYSkRXNJtsBI7D1RirWzAVpOBCCq8Y-fo4jB3LvnvHupiplgdjKNNkPfVKMUE1xT_FyRSScEZaSA_gK7kWtvHzFziZMu9IdisFzBrvGaN1wziUXBz29reHOfvtxP4U9Mx8ua_Pfq2OjuGYpOL9YQxLiUVtGGfDhi00O4iFFNdXIP1sbSDGZ_jv_d4AOXpokM</recordid><startdate>19950327</startdate><enddate>19950327</enddate><creator>Suzuki, Tsutomu</creator><creator>Takamori, Kazuaki</creator><creator>Misawa, Miwa</creator><creator>Onodera, Kenji</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>19950327</creationdate><title>Effects of the histaminergic system on the morphine-induced conditioned place preference in mice</title><author>Suzuki, Tsutomu ; Takamori, Kazuaki ; Misawa, Miwa ; Onodera, Kenji</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c483t-b4a1051bc667df10d1d5883df870e75a215462bfa60cde26087af0a8191525dc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>3,4-Dihydroxyphenylacetic Acid - metabolism</topic><topic>Animals</topic><topic>Behavioral psychophysiology</topic><topic>Benzazepines - pharmacology</topic><topic>Benzothiazoles</topic><topic>Biological and medical sciences</topic><topic>Conditioned place preference</topic><topic>Conditioning, Operant - drug effects</topic><topic>DA turnover</topic><topic>Dihydroxyphenylalanine - metabolism</topic><topic>Dopamine - metabolism</topic><topic>Dose-Response Relationship, Drug</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Histamine - physiology</topic><topic>Histamine H2 Antagonists - pharmacology</topic><topic>Histidine - pharmacology</topic><topic>Histidine Decarboxylase - antagonists & 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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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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