title: The α2-adrenoceptors do not modify the activity of tyrosine hydroxylase, corticoliberine, and neuropeptide Y producing hypothalamic magnocellular neurons ion the Long Evans and Brattleboro rats.
abstract: 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.
authors.affiliation: Laboratory of Functional Neuromorphology, Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovak Republic.
authors.forename: J
authors.initials: J
authors.lastname: Bundzikova
authors.forename: Z
authors.initials: Z
authors.lastname: Pirnik
authors.forename: D
authors.initials: D
authors.lastname: Zelena
authors.forename: J D
authors.initials: JD
authors.lastname: Mikkelsen
authors.forename: A
authors.initials: A
authors.lastname: Kiss
mesh_terms: D058669:Adrenergic alpha-2 Receptor Antagonists / Q000494:pharmacology; D000818:Animals; D003346:Corticotropin-Releasing Hormone / Q000096:biosynthesis / Q000378:metabolism*; D004789:Enzyme Activation / Q000235:genetics / Q000502:physiology; D007031:Hypothalamus / Q000166:cytology / Q000201:enzymology / Q000378:metabolism; D008297:Male; D055495:Neurogenesis / Q000235:genetics / Q000502:physiology*; D009474:Neurons / Q000166:cytology / Q000201:enzymology / Q000378:metabolism*; D009478:Neuropeptide Y / Q000096:biosynthesis / Q000378:metabolism*; D009995:Osmosis / Q000502:physiology; D010286:Paraventricular Hypothalamic Nucleus / Q000201:enzymology / Q000378:metabolism*; D010641:Phenotype; D051381:Rats; D011910:Rats, Brattleboro; D020318:Rats, Long-Evans; D018341:Receptors, Adrenergic, alpha-2 / Q000378:metabolism / Q000502:physiology*; D013495:Supraoptic Nucleus / Q000201:enzymology / Q000378:metabolism*; D014446:Tyrosine 3-Monooxygenase / Q000096:biosynthesis / Q000378:metabolism*; D014667:Vasopressins / Q000172:deficiency / Q000235:genetics
chemical_list: D058669:Adrenergic alpha-2 Receptor Antagonists; D009478:Neuropeptide Y; D018341:Receptors, Adrenergic, alpha-2; D014667:Vasopressins; D003346:Corticotropin-Releasing Hormone; D014446:Tyrosine 3-Monooxygenase