Synergistic effects of dopamine agonists and centrally administered neurotensin on feeding
Several lines of evidence indicate that neruotensin may modulate the activity of dopamine systems in the central nervous system. The present study investigated the possibility that intraperitoneal injections of the dopamine agonists 1-dopa and bromocriptine would alter the aphagia produced by centra...
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| Veröffentlicht in: | Pharmacology, biochemistry and behavior biochemistry and behavior, 1986-05, Vol.24 (5), p.1195-1201 |
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| container_title | Pharmacology, biochemistry and behavior |
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| creator | Hawkins, Mike F. Barkemeyer, Charles A. Tulley, Richard T. |
| description | Several lines of evidence indicate that neruotensin may modulate the activity of dopamine systems in the central nervous system. The present study investigated the possibility that intraperitoneal injections of the dopamine agonists 1-dopa and bromocriptine would alter the aphagia produced by central administration of neurotensin. It was found that neurotensin suppressed feeding in food-deprived rats when injected into the lateral ventricle or the ventromedial hypothalamus. Food intake was not affected, however, when the peptide was placed in the lateral hypothalamus. A dose-dependent aphagia was also observed following peripheral injections of 1-dopa and bromocriptine. Additionally, the anorectic effect of centrally administered neurotensin was potentiated by concurrent administration of doses of 1-dopa or bromocriptine which, when given alone, had no effect on food intake. The data suggest that neurotensin aphagia may be mediated by the peptide's ability to increase the activity of dopamine systems in the central nervous system. |
| doi_str_mv | 10.1016/0091-3057(86)90170-X |
| format | Article |
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The present study investigated the possibility that intraperitoneal injections of the dopamine agonists 1-dopa and bromocriptine would alter the aphagia produced by central administration of neurotensin. It was found that neurotensin suppressed feeding in food-deprived rats when injected into the lateral ventricle or the ventromedial hypothalamus. Food intake was not affected, however, when the peptide was placed in the lateral hypothalamus. A dose-dependent aphagia was also observed following peripheral injections of 1-dopa and bromocriptine. Additionally, the anorectic effect of centrally administered neurotensin was potentiated by concurrent administration of doses of 1-dopa or bromocriptine which, when given alone, had no effect on food intake. The data suggest that neurotensin aphagia may be mediated by the peptide's ability to increase the activity of dopamine systems in the central nervous system.</description><identifier>ISSN: 0091-3057</identifier><identifier>EISSN: 1873-5177</identifier><identifier>DOI: 10.1016/0091-3057(86)90170-X</identifier><identifier>PMID: 3725825</identifier><identifier>CODEN: PBBHAU</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Applied sciences ; Biological and medical sciences ; Bromocriptine ; Bromocriptine - pharmacology ; Catecholaminergic system ; Dopamine - physiology ; Dose-Response Relationship, Drug ; Drug Synergism ; Eating - drug effects ; Exact sciences and technology ; Feeding ; Hypothalamus ; Injections ; Injections, Intraventricular ; Levodopa ; Levodopa - pharmacology ; Male ; Medical sciences ; Neuropharmacology ; Neurotensin ; Neurotensin - pharmacology ; Neurotransmitters. Neurotransmission. Receptors ; Other techniques and industries ; Peptides ; Pharmacology. Drug treatments ; Rats ; Rats, Inbred Strains ; Satiety ; Time Factors</subject><ispartof>Pharmacology, biochemistry and behavior, 1986-05, Vol.24 (5), p.1195-1201</ispartof><rights>1986</rights><rights>1987 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c563t-8684e150775cdae13b0c25002a0c7b55823d3d59818b9e0c0890806d1c0eaa413</citedby><cites>FETCH-LOGICAL-c563t-8684e150775cdae13b0c25002a0c7b55823d3d59818b9e0c0890806d1c0eaa413</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/009130578690170X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8148292$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8184635$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3725825$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hawkins, Mike F.</creatorcontrib><creatorcontrib>Barkemeyer, Charles A.</creatorcontrib><creatorcontrib>Tulley, Richard T.</creatorcontrib><title>Synergistic effects of dopamine agonists and centrally administered neurotensin on feeding</title><title>Pharmacology, biochemistry and behavior</title><addtitle>Pharmacol Biochem Behav</addtitle><description>Several lines of evidence indicate that neruotensin may modulate the activity of dopamine systems in the central nervous system. The present study investigated the possibility that intraperitoneal injections of the dopamine agonists 1-dopa and bromocriptine would alter the aphagia produced by central administration of neurotensin. It was found that neurotensin suppressed feeding in food-deprived rats when injected into the lateral ventricle or the ventromedial hypothalamus. Food intake was not affected, however, when the peptide was placed in the lateral hypothalamus. A dose-dependent aphagia was also observed following peripheral injections of 1-dopa and bromocriptine. Additionally, the anorectic effect of centrally administered neurotensin was potentiated by concurrent administration of doses of 1-dopa or bromocriptine which, when given alone, had no effect on food intake. The data suggest that neurotensin aphagia may be mediated by the peptide's ability to increase the activity of dopamine systems in the central nervous system.</description><subject>Animals</subject><subject>Applied sciences</subject><subject>Biological and medical sciences</subject><subject>Bromocriptine</subject><subject>Bromocriptine - pharmacology</subject><subject>Catecholaminergic system</subject><subject>Dopamine - physiology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Synergism</subject><subject>Eating - drug effects</subject><subject>Exact sciences and technology</subject><subject>Feeding</subject><subject>Hypothalamus</subject><subject>Injections</subject><subject>Injections, Intraventricular</subject><subject>Levodopa</subject><subject>Levodopa - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neuropharmacology</subject><subject>Neurotensin</subject><subject>Neurotensin - pharmacology</subject><subject>Neurotransmitters. Neurotransmission. Receptors</subject><subject>Other techniques and industries</subject><subject>Peptides</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Satiety</subject><subject>Time Factors</subject><issn>0091-3057</issn><issn>1873-5177</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1986</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUtrGzEURkVoSB0n_yABLUpIFpNejUYjzaZQQl4QyCINhG6ELN0xKmPJlcYB__vItfGyZHVB37kPjgg5Y3DNgLXfATpWcRDyUrVXHTAJ1dsBmTAleSWYlF_IZI98Jcc5_wGApm7lETnishaqFhPy-2UdMM19Hr2l2Pdox0xjT11cmoUPSM08hpJmaoKjFsOYzDCsqXElLe-Y0NGAqxRHDNkHGgPtEZ0P8xNy2Jsh4-muTsnr3e2vm4fq6fn-8ebnU2VFy8dKtapBJkBKYZ1BxmdgawFQG7ByJsqZ3HEnOsXUrEOwoDpQ0DpmAY1pGJ-Si-3cZYp_V5hHvfDZ4jCYgHGVNWuaWm2sTEmzBW2KOSfs9TL5hUlrzUBvlOqNL73xpVWr_ynVb6XtfDd_NVug2zftHJb82y432ZqhTyZYn_dYWd20_BNYo-quLtiPLYZF2bvHpLP1GGxRmsrnaBf9_8_9ABzen1o</recordid><startdate>19860501</startdate><enddate>19860501</enddate><creator>Hawkins, Mike F.</creator><creator>Barkemeyer, Charles A.</creator><creator>Tulley, Richard T.</creator><general>Elsevier Inc</general><general>Elsevier Science</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></search><sort><creationdate>19860501</creationdate><title>Synergistic effects of dopamine agonists and centrally administered neurotensin on feeding</title><author>Hawkins, Mike F. ; Barkemeyer, Charles A. ; Tulley, Richard T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c563t-8684e150775cdae13b0c25002a0c7b55823d3d59818b9e0c0890806d1c0eaa413</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1986</creationdate><topic>Animals</topic><topic>Applied sciences</topic><topic>Biological and medical sciences</topic><topic>Bromocriptine</topic><topic>Bromocriptine - pharmacology</topic><topic>Catecholaminergic system</topic><topic>Dopamine - physiology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Synergism</topic><topic>Eating - drug effects</topic><topic>Exact sciences and technology</topic><topic>Feeding</topic><topic>Hypothalamus</topic><topic>Injections</topic><topic>Injections, Intraventricular</topic><topic>Levodopa</topic><topic>Levodopa - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neuropharmacology</topic><topic>Neurotensin</topic><topic>Neurotensin - pharmacology</topic><topic>Neurotransmitters. Neurotransmission. Receptors</topic><topic>Other techniques and industries</topic><topic>Peptides</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Satiety</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hawkins, Mike F.</creatorcontrib><creatorcontrib>Barkemeyer, Charles A.</creatorcontrib><creatorcontrib>Tulley, Richard T.</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><jtitle>Pharmacology, biochemistry and behavior</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hawkins, Mike F.</au><au>Barkemeyer, Charles A.</au><au>Tulley, Richard T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Synergistic effects of dopamine agonists and centrally administered neurotensin on feeding</atitle><jtitle>Pharmacology, biochemistry and behavior</jtitle><addtitle>Pharmacol Biochem Behav</addtitle><date>1986-05-01</date><risdate>1986</risdate><volume>24</volume><issue>5</issue><spage>1195</spage><epage>1201</epage><pages>1195-1201</pages><issn>0091-3057</issn><eissn>1873-5177</eissn><coden>PBBHAU</coden><abstract>Several lines of evidence indicate that neruotensin may modulate the activity of dopamine systems in the central nervous system. The present study investigated the possibility that intraperitoneal injections of the dopamine agonists 1-dopa and bromocriptine would alter the aphagia produced by central administration of neurotensin. It was found that neurotensin suppressed feeding in food-deprived rats when injected into the lateral ventricle or the ventromedial hypothalamus. Food intake was not affected, however, when the peptide was placed in the lateral hypothalamus. A dose-dependent aphagia was also observed following peripheral injections of 1-dopa and bromocriptine. Additionally, the anorectic effect of centrally administered neurotensin was potentiated by concurrent administration of doses of 1-dopa or bromocriptine which, when given alone, had no effect on food intake. The data suggest that neurotensin aphagia may be mediated by the peptide's ability to increase the activity of dopamine systems in the central nervous system.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>3725825</pmid><doi>10.1016/0091-3057(86)90170-X</doi><tpages>7</tpages></addata></record> |
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| ispartof | Pharmacology, biochemistry and behavior, 1986-05, Vol.24 (5), p.1195-1201 |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Animals Applied sciences Biological and medical sciences Bromocriptine Bromocriptine - pharmacology Catecholaminergic system Dopamine - physiology Dose-Response Relationship, Drug Drug Synergism Eating - drug effects Exact sciences and technology Feeding Hypothalamus Injections Injections, Intraventricular Levodopa Levodopa - pharmacology Male Medical sciences Neuropharmacology Neurotensin Neurotensin - pharmacology Neurotransmitters. Neurotransmission. Receptors Other techniques and industries Peptides Pharmacology. Drug treatments Rats Rats, Inbred Strains Satiety Time Factors |
| title | Synergistic effects of dopamine agonists and centrally administered neurotensin on feeding |
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