Linked Life Data

20814066

Source:http://linkedlifedata.com/resource/pubmed/id/20814066

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2010-9-3
pubmed:abstractText
The hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei are activated by body salt-fluid variations. Stimulation of alpha(2)-adrenoceptors by an agonist-xylazine (XYL) activates oxytocinergic but not vasopressinergic magnocellular neurons. In this study, tyrosine hydroxylase (TH), corticoliberine (CRH), and neuropeptide Y(NPY) magnocellular phenotypes, were analysed in response to alpha(2)-adrenoceptor manipulations and sustained hyperosmolality in vasopressin deficient homozygous Brattleboro (di/di) rats. Saline (0.9% NaCl, 0.1 ml/100g/bw), XYL (10 mg/kg/bw), atipamezole (ATIP, alpha(2)-adrenoceptors antagonist, 1 mg/kg/bw), and ATIP 5 min later followed by XYL, were applied intraperitoneally. Presence of immunolabeled Fos peptide signalized the neuronal activity. Ninety minutes after injections, the rats were anesthesized and sacrificed by transcardial perfusion with fixative. Coronal sections of 30 mum thickness double immunolabeled with Fos/neuropeptide were evaluated under light microscope. Under basal conditions, di/di in comparison with control Long Evans rats, displayed significantly higher number of TH, CRH, and NPY immunoreactive neurons in the SON and PVN (except NPY cells in PVN) and more than 90%, 75%, and 86% of TH, NPY, and CRH neurons, respectively, displayed also Fos signal in the SON. XYL did not further increase the number of Fos in the PVN and SON and ATIP failed to reduce the stimulatory effect of hypertonic saline in all neuronal phenotypes studied. Our data indicate that hyperosmotic conditions significantly influence the activity of TH, CRH, and NPY magnocellular neuronal phenotypes, but alpha(2)-adrenoceptors do not play substantial role in their regulation during osmotic challenge induced by AVP deficiency.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1899-1505
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
61
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
391-8
pubmed:meshHeading
pubmed-meshheading:20814066-Adrenergic alpha-2 Receptor Antagonists, pubmed-meshheading:20814066-Animals, pubmed-meshheading:20814066-Corticotropin-Releasing Hormone, pubmed-meshheading:20814066-Enzyme Activation, pubmed-meshheading:20814066-Hypothalamus, pubmed-meshheading:20814066-Male, pubmed-meshheading:20814066-Neurogenesis, pubmed-meshheading:20814066-Neurons, pubmed-meshheading:20814066-Neuropeptide Y, pubmed-meshheading:20814066-Osmosis, pubmed-meshheading:20814066-Paraventricular Hypothalamic Nucleus, pubmed-meshheading:20814066-Phenotype, pubmed-meshheading:20814066-Rats, pubmed-meshheading:20814066-Rats, Brattleboro, pubmed-meshheading:20814066-Rats, Long-Evans, pubmed-meshheading:20814066-Receptors, Adrenergic, alpha-2, pubmed-meshheading:20814066-Supraoptic Nucleus, pubmed-meshheading:20814066-Tyrosine 3-Monooxygenase, pubmed-meshheading:20814066-Vasopressins
pubmed:year
2010
pubmed:articleTitle
The ?2-adrenoceptors do not modify the activity of tyrosine hydroxylase, corticoliberine, and neuropeptide Y producing hypothalamic magnocellular neurons ion the Long Evans and Brattleboro rats.
pubmed:affiliation
Laboratory of Functional Neuromorphology, Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovak Republic.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't