Publication:
CDP-choline increases plasma ACTH and potentiates the stimulated release of GH, TSH and LH: the cholinergic involvement

dc.contributor.buuauthorÇavun, Sinan
dc.contributor.buuauthorSavcı, Vahide
dc.contributor.departmentTıp Fakültesi
dc.contributor.departmentTıbbi Farmakoloji Ana Bilim Dalı
dc.contributor.researcheridAAC-9702-2019
dc.contributor.scopusid6507468595
dc.contributor.scopusid6603687024
dc.date.accessioned2022-03-14T12:56:35Z
dc.date.available2022-03-14T12:56:35Z
dc.date.issued2004-10
dc.description.abstractIn the present study, we investigated the effect of intracerebroventricular (i.c.v.) administration of cytidine-5′-diphosphate (CDP) choline on plasma adrenocorticotropin (ACTH), serum growth hormone (GH), thyroid stimulating hormone (TSH), follicle stimulating hormone (FSH) and luteinizing hormone (LH) levels in conscious rats. The involvement of cholinergic mechanisms in these effects was also determined. In basal conditions, CDP-choline (0.5, 1.0 and 2.0 μmol, i.c.v.) increased plasma ACTH levels dose- and time-dependently, but it did not affect the TSH, GH, FSH and LH levels. In stimulated conditions, i.c.v. administration of CDP-choline (1 μmol, i.c.v.) produced an increase in clonidine-stimulated GH, thyrotyropin-releasing hormone (TRH)-stimulated TSH, LH-releasing hormone (LHRH)-stimulated LH, but not FSH levels. Injection of equimolar dose of choline (1 μmol, i.c.v.) produced similar effects on hormone levels, but cytidine (1 μmol, i.c.v.) failed to alter plasma levels of these hormones. Pretreatment with hemicholinium-3, a neuronal high affinity choline uptake inhibitor, (20 μg, i.c.v.) completely blocked the observed hormone responses to CDP-choline. The increase in plasma ACTH levels induced by CDP-choline (1 μmol, i.c.v.) was abolished by pretreatment with mecamylamine, a nicotinic receptor antagonist, (50 μg, i.c.v.) but not atropine, a muscarinic receptor antagonist, (10 μg, i.c.v.). The increase in stimulated levels of serum TSH by CDP-choline (1 μmol, i.c.v.) was blocked by atropine but not by mecamylamine pretreatment. However, CDP-choline induced increases in serum GH and LH levels were greatly attenuated by both atropine and mecamylamine pretreatments. The results show that CDP-choline can increase plasma ACTH and produce additional increases in serum levels of TSH, GH and LH stimulated by TRH, clonidine and LHRH, respectively. The activation of central cholinergic system, mainly through the presynaptic mechanisms, was involved in these effects. Central nicotinic receptors solely mediated the increase in plasma ACTH levels while the activation of central muscarinic receptors was involved in the increase in TSH levels. Both muscarinic and nicotinic receptor activations, separately, mediated the increases in serum GH and LH levels after CDP-choline.
dc.identifier.citationÇavun, S. ve Savcı, V. (2004). “CDP-choline increases plasma ACTH and potentiates the stimulated release of GH, TSH and LH: The cholinergic involvement”. Fundamental and Clinical Pharmacology, 18(5), 513-523.
dc.identifier.endpage523
dc.identifier.issn0767-3981
dc.identifier.issue5
dc.identifier.pubmed15482372
dc.identifier.scopus2-s2.0-7944227782
dc.identifier.startpage513
dc.identifier.urihttps://doi.org/10.1111/j.1472-8206.2004.00272.x
dc.identifier.urihttps://onlinelibrary.wiley.com/doi/10.1111/j.1472-8206.2004.00272.x
dc.identifier.urihttp://hdl.handle.net/11452/25003
dc.identifier.volume18
dc.identifier.wos000225007800002
dc.indexed.wosSCIE
dc.language.isoen
dc.publisherWiley
dc.relation.journalFundamental and Clinical Pharmacology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectPharmacology and pharmacy
dc.subjectAdrenocorticotropin
dc.subjectCholinergic
dc.subjectCytidine-5′-diphosphate choline
dc.subjectGrowth hormone
dc.subjectLuteinizing hormone
dc.subjectThyroid stimulating hormone
dc.subjectGrowth-hormone-secretion
dc.subjectConscious rats
dc.subjectAcetylcholine-receptors
dc.subjectIntracerebroventricular injection
dc.subjectNeuroendocrine control
dc.subjectCerebral-ischemia
dc.subjectNeurons
dc.subjectActivation
dc.subjectBrain
dc.subject.emtreeAtropine
dc.subject.emtreeCholine
dc.subject.emtreeCiticoline
dc.subject.emtreeClonidine
dc.subject.emtreeCorticotropin
dc.subject.emtreeFollitropin
dc.subject.emtreeGonadorelin
dc.subject.emtreeGrowth hormone
dc.subject.emtreeHemicholinium 3
dc.subject.emtreeLuteinizing hormone
dc.subject.emtreeMecamylamine
dc.subject.emtreeMuscarinic receptor
dc.subject.emtreeMuscarinic receptor blocking agent
dc.subject.emtreeNicotinic receptor
dc.subject.emtreeNicotinic receptor blocking agent
dc.subject.emtreeProtirelin
dc.subject.emtreeThyrotropin
dc.subject.emtreeAnimal experiment
dc.subject.emtreeArticle
dc.subject.emtreeCholinergic system
dc.subject.emtreeControlled study
dc.subject.emtreeCorticotropin blood level
dc.subject.emtreeDose response
dc.subject.emtreeDose time effect relation
dc.subject.emtreeDrug effect
dc.subject.emtreeFollitropin blood level
dc.subject.emtreeGrowth hormone blood level
dc.subject.emtreeGrowth hormone release
dc.subject.emtreeLuteinizing hormone blood level
dc.subject.emtreeLuteinizing hormone release
dc.subject.emtreeMale
dc.subject.emtreeNonhuman
dc.subject.emtreePresynaptic nerve
dc.subject.emtreePriority journal
dc.subject.emtreeRat
dc.subject.emtreeReceptor upregulation
dc.subject.emtreeThyrotropin blood level
dc.subject.emtreeThyrotropin release
dc.subject.meshAdrenocorticotropic hormone
dc.subject.meshAnimals
dc.subject.meshCytidine diphosphate choline
dc.subject.meshFollicle stimulating hormone
dc.subject.meshGrowth hormone
dc.subject.meshInjections, intraventricular
dc.subject.meshLuteinizing hormone
dc.subject.meshMale
dc.subject.meshRats
dc.subject.meshRats, wistar
dc.subject.meshThyrotropin
dc.subject.meshTime factors
dc.subject.scopusCiticoline; Brain Ischemia; Glycerylphosphorylcholine
dc.subject.wosPharmacology and pharmacy
dc.titleCDP-choline increases plasma ACTH and potentiates the stimulated release of GH, TSH and LH: the cholinergic involvement
dc.typeArticle
dc.wos.quartileQ3
dspace.entity.typePublication
local.contributor.departmentTıp Fakültesi/Tıbbi Farmakoloji Ana Bilim Dalı
local.indexed.atScopus
local.indexed.atWOS

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