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Status: Bibliographieeintrag

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Verfasst von:Culman, Juraj [VerfasserIn]   i
 Das, G. [VerfasserIn]   i
 Ohlendorf, C. [VerfasserIn]   i
 Haass, Markus [VerfasserIn]   i
 Maser-Gluth, Christiane [VerfasserIn]   i
 Zuhayra, M. [VerfasserIn]   i
 Zhao, Y. [VerfasserIn]   i
 Itoi, K. [VerfasserIn]   i
Titel:Blockade of tachykinin NK1/NK2 receptors in the brain attenuates the activation of corticotrophin-releasing hormone neurones in the hypothalamic paraventricular nucleus and the sympathoadrenal and pituitary-adrenal responses to formalin-induced pain in the rat
Verf.angabe:J. Culman, G. Das, C. Ohlendorf, M. Haass, C. Maser-Gluth, M. Zuhayra, Y. Zhao and K. Itoi
E-Jahr:2010
Jahr:19 April 2010
Umfang:10 S.
Illustrationen:Illustrationen
Fussnoten:Gesehen am 21.07.2023
Titel Quelle:Enthalten in: Journal of neuroendocrinology
Ort Quelle:Oxford [u.a.] : Wiley-Blackwell, 1989
Jahr Quelle:2010
Band/Heft Quelle:22(2010), 5 vom: Mai, Seite 467-476
ISSN Quelle:1365-2826
Abstract:Evidence from pharmacological studies has implicated substance P (SP), a natural ligand of tachykinin NK(1) receptors which can also interact with NK(2) receptors, in the generation of pressor and tachycardic responses to stress. Using selective blockade of brain NK(1) and NK(2) receptors, we tested in conscious rats the hypothesis that SP initiates, within the neuronal brain circuits, the sympathoadrenal, hypothalamic-pituitary-adrenal (HPA) and behavioural responses to noxious stimuli. Formalin injected s.c. through a chronically implanted catheter in the area of the lower leg was used as a pain stimulus. Rats were pretreated i.c.v. with vehicle or the selective, nonpeptide antagonists of tachykinin NK(1) and NK(2) receptors, RP 67580 and SR 48968, respectively. Ten minutes thereafter, formalin was injected s.c. and the cardiovascular responses were recorded, plasma concentrations of catecholamines, adrenocorticotrophic hormone (ACTH) and corticosterone were determined and the expression of the inducible transcription factor c-Fos in the paraventricular (PVN) and supraoptic nuclei was detected to identify neurones which were activated during pain stimulation. Blockade of NK(1) and NK(2) receptors attenuated the formalin-induced increases in mean arterial pressure and heart rate, adrenaline and ACTH concentrations in plasma, and completely abolished the pain-induced c-Fos expression in corticotrophin-releasing hormone neurones localised in the parvocellular division of the PVN. The results obtained provide pharmacological evidence that tachykinins, most probably SP, act as mediators within the neuronal circuits linked to the initiation and control of the cardiovascular, sympathoadrenal, HPA and behavioural responses to pain stimuli and provide an excitatory input to corticotrophin-releasing hormone neurones in the PVN to activate the HPA axis. Our data demonstrating the inhibition of the complex response pattern to noxious stimuli and stress are consistent with the proposed anxiolytic and antidepressant activity of NK(1) and NK(2) receptor antagonists.
DOI:doi:10.1111/j.1365-2826.2010.01987.x
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.1111/j.1365-2826.2010.01987.x
 DOI: https://doi.org/10.1111/j.1365-2826.2010.01987.x
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Animals
 Blood Pressure
 Brain
 Corticotropin-Releasing Hormone
 Formaldehyde
 Heart Rate
 Neurons
 Pain
 Paraventricular Hypothalamic Nucleus
 Pituitary-Adrenal System
 Rats
 Receptors, Tachykinin
K10plus-PPN:1853356018
Verknüpfungen:→ Zeitschrift

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