Altered pain sensitivity and morphine-induced anti-nociception in mice lacking CCK2 receptors
Cholecystokinin (CCK) interacts with the endopioid system in the regulation of various physiological functions, including the control of pain sensitivity, motor activity and emotional behaviour. The aim of the present work was to study the pain sensitivity, morphine-induced antinociception and densi...
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| Veröffentlicht in: | Psychopharmacologia 2003-03, Vol.166 (2), p.168-175 |
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| creator | VERAKSITS, Alar RÜNKORG, Kertu KURRIKOFF, Kaido RAUD, Sirli ABRAMOV, Urho MATSUI, Toshimitsu BOURIN, Michel KOKS, Sulev VASAR, Eero |
| description | Cholecystokinin (CCK) interacts with the endopioid system in the regulation of various physiological functions, including the control of pain sensitivity, motor activity and emotional behaviour.
The aim of the present work was to study the pain sensitivity, morphine-induced antinociception and density of opioid receptors in mice lacking CCK(2) receptors.
Plantar analgesia and hotplate tests were used to evaluate pain sensitivity and morphine-induced antinociception. The parameters of opioid receptors were analysed by using [(3)H]-diprenorphine binding.
In the plantar analgesia test the latency of hind paw withdrawal was significantly increased in CCK(2) receptor deficient mice compared to wild-type (+/+) littermates. The treatment with saline reversed the reduced pain sensitivity in heterozygous (+/-) and homozygous (-/-) mice. The administration of morphine (1 mg/kg) induced a significantly stronger antinociceptive effect in homozygous (-/-) mice compared with wild-type (+/+) animals. In the hotplate test, only homozygous (-/-) mutant mice displayed the delayed latency of hind paw licking/shaking in comparison with wild-type (+/+) mice. The injection of saline and isolation of mice for 30 min reversed the delayed response in homozygous (-/-) mice. However, in this test, the anti-nociceptive action of morphine (5-10 mg/kg) in mutant mice did not differ from that in wild-type (+/+) littermates. By contrast, the jump latency was decreased in both homozygous (-/-) and heterozygous (+/-) mice in the hotplate test. The increased density of opioid receptors was established in the striatum of homozygous (-/-) mice.
It is apparent that the targeted mutagenesis of the CCK(2) receptor gene has different effects on the sensitivity of opioid receptors in various brain structures. This is a probable reason for the altered pain sensitivity and morphine-induced antinociception in mutant mice compared to wild-type (+/+) littermates. |
| doi_str_mv | 10.1007/s00213-002-1333-6 |
| format | Article |
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The aim of the present work was to study the pain sensitivity, morphine-induced antinociception and density of opioid receptors in mice lacking CCK(2) receptors.
Plantar analgesia and hotplate tests were used to evaluate pain sensitivity and morphine-induced antinociception. The parameters of opioid receptors were analysed by using [(3)H]-diprenorphine binding.
In the plantar analgesia test the latency of hind paw withdrawal was significantly increased in CCK(2) receptor deficient mice compared to wild-type (+/+) littermates. The treatment with saline reversed the reduced pain sensitivity in heterozygous (+/-) and homozygous (-/-) mice. The administration of morphine (1 mg/kg) induced a significantly stronger antinociceptive effect in homozygous (-/-) mice compared with wild-type (+/+) animals. In the hotplate test, only homozygous (-/-) mutant mice displayed the delayed latency of hind paw licking/shaking in comparison with wild-type (+/+) mice. The injection of saline and isolation of mice for 30 min reversed the delayed response in homozygous (-/-) mice. However, in this test, the anti-nociceptive action of morphine (5-10 mg/kg) in mutant mice did not differ from that in wild-type (+/+) littermates. By contrast, the jump latency was decreased in both homozygous (-/-) and heterozygous (+/-) mice in the hotplate test. The increased density of opioid receptors was established in the striatum of homozygous (-/-) mice.
It is apparent that the targeted mutagenesis of the CCK(2) receptor gene has different effects on the sensitivity of opioid receptors in various brain structures. This is a probable reason for the altered pain sensitivity and morphine-induced antinociception in mutant mice compared to wild-type (+/+) littermates.</description><identifier>ISSN: 0033-3158</identifier><identifier>EISSN: 1432-2072</identifier><identifier>DOI: 10.1007/s00213-002-1333-6</identifier><identifier>PMID: 12545332</identifier><identifier>CODEN: PSYPAG</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Analgesics ; Analgesics, Opioid - pharmacology ; Animals ; Biological and medical sciences ; Diprenorphine - metabolism ; Drug withdrawal ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Morphine ; Morphine - pharmacology ; Mutagenesis ; Narcotics ; Neuropeptides ; Neuropharmacology ; Pain ; Pain Threshold - drug effects ; Peptides ; Pharmacology. Drug treatments ; Physiology ; Radioligand Assay ; Receptor, Cholecystokinin B ; Receptors, Cholecystokinin - physiology</subject><ispartof>Psychopharmacologia, 2003-03, Vol.166 (2), p.168-175</ispartof><rights>2003 INIST-CNRS</rights><rights>Copyright Springer-Verlag 2003</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c354t-b0f9a5d3c5997d5827765b8469e63fcd3788c933f307c8522e42c55ec9eeb4fe3</citedby><cites>FETCH-LOGICAL-c354t-b0f9a5d3c5997d5827765b8469e63fcd3788c933f307c8522e42c55ec9eeb4fe3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14560462$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12545332$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>VERAKSITS, Alar</creatorcontrib><creatorcontrib>RÜNKORG, Kertu</creatorcontrib><creatorcontrib>KURRIKOFF, Kaido</creatorcontrib><creatorcontrib>RAUD, Sirli</creatorcontrib><creatorcontrib>ABRAMOV, Urho</creatorcontrib><creatorcontrib>MATSUI, Toshimitsu</creatorcontrib><creatorcontrib>BOURIN, Michel</creatorcontrib><creatorcontrib>KOKS, Sulev</creatorcontrib><creatorcontrib>VASAR, Eero</creatorcontrib><title>Altered pain sensitivity and morphine-induced anti-nociception in mice lacking CCK2 receptors</title><title>Psychopharmacologia</title><addtitle>Psychopharmacology (Berl)</addtitle><description>Cholecystokinin (CCK) interacts with the endopioid system in the regulation of various physiological functions, including the control of pain sensitivity, motor activity and emotional behaviour.
The aim of the present work was to study the pain sensitivity, morphine-induced antinociception and density of opioid receptors in mice lacking CCK(2) receptors.
Plantar analgesia and hotplate tests were used to evaluate pain sensitivity and morphine-induced antinociception. The parameters of opioid receptors were analysed by using [(3)H]-diprenorphine binding.
In the plantar analgesia test the latency of hind paw withdrawal was significantly increased in CCK(2) receptor deficient mice compared to wild-type (+/+) littermates. The treatment with saline reversed the reduced pain sensitivity in heterozygous (+/-) and homozygous (-/-) mice. The administration of morphine (1 mg/kg) induced a significantly stronger antinociceptive effect in homozygous (-/-) mice compared with wild-type (+/+) animals. In the hotplate test, only homozygous (-/-) mutant mice displayed the delayed latency of hind paw licking/shaking in comparison with wild-type (+/+) mice. The injection of saline and isolation of mice for 30 min reversed the delayed response in homozygous (-/-) mice. However, in this test, the anti-nociceptive action of morphine (5-10 mg/kg) in mutant mice did not differ from that in wild-type (+/+) littermates. By contrast, the jump latency was decreased in both homozygous (-/-) and heterozygous (+/-) mice in the hotplate test. The increased density of opioid receptors was established in the striatum of homozygous (-/-) mice.
It is apparent that the targeted mutagenesis of the CCK(2) receptor gene has different effects on the sensitivity of opioid receptors in various brain structures. This is a probable reason for the altered pain sensitivity and morphine-induced antinociception in mutant mice compared to wild-type (+/+) littermates.</description><subject>Analgesics</subject><subject>Analgesics, Opioid - pharmacology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Diprenorphine - metabolism</subject><subject>Drug withdrawal</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Morphine</subject><subject>Morphine - pharmacology</subject><subject>Mutagenesis</subject><subject>Narcotics</subject><subject>Neuropeptides</subject><subject>Neuropharmacology</subject><subject>Pain</subject><subject>Pain Threshold - drug effects</subject><subject>Peptides</subject><subject>Pharmacology. 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Drug treatments</topic><topic>Physiology</topic><topic>Radioligand Assay</topic><topic>Receptor, Cholecystokinin B</topic><topic>Receptors, Cholecystokinin - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>VERAKSITS, Alar</creatorcontrib><creatorcontrib>RÜNKORG, Kertu</creatorcontrib><creatorcontrib>KURRIKOFF, Kaido</creatorcontrib><creatorcontrib>RAUD, Sirli</creatorcontrib><creatorcontrib>ABRAMOV, Urho</creatorcontrib><creatorcontrib>MATSUI, Toshimitsu</creatorcontrib><creatorcontrib>BOURIN, Michel</creatorcontrib><creatorcontrib>KOKS, Sulev</creatorcontrib><creatorcontrib>VASAR, Eero</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>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><jtitle>Psychopharmacologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>VERAKSITS, Alar</au><au>RÜNKORG, Kertu</au><au>KURRIKOFF, Kaido</au><au>RAUD, Sirli</au><au>ABRAMOV, Urho</au><au>MATSUI, Toshimitsu</au><au>BOURIN, Michel</au><au>KOKS, Sulev</au><au>VASAR, Eero</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Altered pain sensitivity and morphine-induced anti-nociception in mice lacking CCK2 receptors</atitle><jtitle>Psychopharmacologia</jtitle><addtitle>Psychopharmacology (Berl)</addtitle><date>2003-03-01</date><risdate>2003</risdate><volume>166</volume><issue>2</issue><spage>168</spage><epage>175</epage><pages>168-175</pages><issn>0033-3158</issn><eissn>1432-2072</eissn><coden>PSYPAG</coden><abstract>Cholecystokinin (CCK) interacts with the endopioid system in the regulation of various physiological functions, including the control of pain sensitivity, motor activity and emotional behaviour.
The aim of the present work was to study the pain sensitivity, morphine-induced antinociception and density of opioid receptors in mice lacking CCK(2) receptors.
Plantar analgesia and hotplate tests were used to evaluate pain sensitivity and morphine-induced antinociception. The parameters of opioid receptors were analysed by using [(3)H]-diprenorphine binding.
In the plantar analgesia test the latency of hind paw withdrawal was significantly increased in CCK(2) receptor deficient mice compared to wild-type (+/+) littermates. The treatment with saline reversed the reduced pain sensitivity in heterozygous (+/-) and homozygous (-/-) mice. The administration of morphine (1 mg/kg) induced a significantly stronger antinociceptive effect in homozygous (-/-) mice compared with wild-type (+/+) animals. In the hotplate test, only homozygous (-/-) mutant mice displayed the delayed latency of hind paw licking/shaking in comparison with wild-type (+/+) mice. The injection of saline and isolation of mice for 30 min reversed the delayed response in homozygous (-/-) mice. However, in this test, the anti-nociceptive action of morphine (5-10 mg/kg) in mutant mice did not differ from that in wild-type (+/+) littermates. By contrast, the jump latency was decreased in both homozygous (-/-) and heterozygous (+/-) mice in the hotplate test. The increased density of opioid receptors was established in the striatum of homozygous (-/-) mice.
It is apparent that the targeted mutagenesis of the CCK(2) receptor gene has different effects on the sensitivity of opioid receptors in various brain structures. This is a probable reason for the altered pain sensitivity and morphine-induced antinociception in mutant mice compared to wild-type (+/+) littermates.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>12545332</pmid><doi>10.1007/s00213-002-1333-6</doi><tpages>8</tpages></addata></record> |
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| ispartof | Psychopharmacologia, 2003-03, Vol.166 (2), p.168-175 |
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| subjects | Analgesics Analgesics, Opioid - pharmacology Animals Biological and medical sciences Diprenorphine - metabolism Drug withdrawal Medical sciences Mice Mice, Inbred C57BL Morphine Morphine - pharmacology Mutagenesis Narcotics Neuropeptides Neuropharmacology Pain Pain Threshold - drug effects Peptides Pharmacology. Drug treatments Physiology Radioligand Assay Receptor, Cholecystokinin B Receptors, Cholecystokinin - physiology |
| title | Altered pain sensitivity and morphine-induced anti-nociception in mice lacking CCK2 receptors |
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