Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/10715
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dc.contributor.authorMussa, Bashair Men
dc.contributor.authorSartor, Daniela Men
dc.contributor.authorVerberne, Anthony J Men
dc.date.accessioned2015-05-16T00:15:17Z
dc.date.available2015-05-16T00:15:17Z
dc.date.issued2008-11-09en
dc.identifier.citationEuropean Journal of Pharmacology 2008; 601(1-3): 198-206en
dc.identifier.govdoc19026634en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/10715en
dc.description.abstractCholecystokinin and serotonin are released from the gastrointestinal tract in response to the products of digestion and play critical roles in mediating pancreatic secretion via vago-vagal reflex pathways. This study was designed to investigate the effects of activation of cholecystokinin CCK(1) and serotonin (5-hydroxytryptamine, 5-HT) 5-HT(3) receptors on pancreatic vagal afferent discharge and to determine whether there is an interaction between these receptors. Male Sprague Dawley rats anaesthetised with isoflurane (1.5%/100% O(2)) were used in all experiments. The effects of systemic administration of cholecystokinin and the serotonin 5-HT(3) receptor agonist phenylbiguanide on pancreatic vagal afferent discharge were recorded before and after administration of cholecystokinin CCK(1) and serotonin 5-HT(3) receptor antagonists. Cholecystokinin (0.1-10 microg/kg, i.v.) and phenylbiguanide (1 and 10 microg/kg, i.v.) increased pancreatic vagal afferent discharge dose-dependently. Cholecystokinin CCK(1) receptor antagonists, lorglumide (10 mg/kg, i.v.) and devazepide (0.5 mg/kg, i.v.), reduced cholecystokinin- and phenylbiguanide-induced increases in pancreatic vagal afferent discharge significantly (n=5, P<0.05). On the other hand, serotonin 5-HT(3) receptor blockade with granisetron (1 mg/kg, i.v.) or MDL72222 ([(1S,5R)-8-methyl-8-azabicyclo[3.2.1]octan-3-yl] 3,5-dichlorobenzoate; 0.1 mg/kg, i.v.) inhibited the pancreatic vagal afferent discharge responses to phenylbiguanide but not those to cholecystokinin. This study has confirmed that cholecystokinin and phenylbiguanide activate pancreatic vagal afferent discharge via activation of cholecystokinin CCK(1) and serotonin 5-HT(3) receptors, respectively. In addition, it has demonstrated that (i) the serotonin 5-HT(3) agonist phenylbiguanide acts partly via an interaction with cholecystokinin CCK(1) receptors, and (ii) the actions of cholecystokinin are not dependent on serotonin 5-HT(3) receptor activation.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherBiguanides.administration & dosage.pharmacologyen
dc.subject.otherCholecystokinin.administration & dosage.metabolismen
dc.subject.otherDose-Response Relationship, Drugen
dc.subject.otherMaleen
dc.subject.otherNeurons, Afferent.metabolismen
dc.subject.otherPancreas.innervation.metabolismen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherReceptor, Cholecystokinin A.drug effects.metabolismen
dc.subject.otherReceptors, Serotonin, 5-HT3.drug effects.metabolismen
dc.subject.otherSerotonin Receptor Agonists.administration & dosage.pharmacologyen
dc.subject.otherVagus Nerve.metabolismen
dc.titleActivation of cholecystokinin (CCK 1) and serotonin (5-HT 3) receptors increases the discharge of pancreatic vagal afferents.en
dc.typeJournal Articleen
dc.identifier.journaltitleEuropean Journal of Pharmacologyen
dc.identifier.affiliationUniversity of Melbourne, Department of Medicine, Clinical Pharmacology and Therapeutics Unit, Austin Health, Heidelberg 3084, Victoria, Australiaen
dc.identifier.doi10.1016/j.ejphar.2008.11.007en
dc.description.pages198-206en
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pubmed/19026634en
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