Domperidone stimulates prolactin secretion in rats with complete destruction of the mediobasal hypothalamus

D. T. Kiem, Gy M. Nagy, I. Barna, G. Makara

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

The main objective of this study was to further elucidate the functional relationship between endogenous dopamine and the prolactin (PRL)-releasing effect of the dopamine antagonists domperidone and haloperidol. We studied the effect of the above dopamine antagonists on the PRL secretion in control and mediobasal hypothalamus (MBH)-lesioned rats. Significant increase in basal plasma PRL levels was detected 7 days after complete surgical destruction of the MBH. Haloperidol injection (0.5 mg/kg, IV) was followed by an increased plasma PRL concentration in the sham-operated animals; however, in the MBH-lesioned rats where the basal PRL levels were high haloperidol failed to produce additional PRL release. In contrast to haloperidol, domperidone (0.1 mg/kg, IV) was able to further elevate the MBH-lesion induced high plasma PRL concentration. Moreover, the change in plasma PRL levels of the MBH-lesioned rats was parallel with that in the sham-lesioned animals after domperidone injections. When haloperidol was given prior to the domperidone injection it did not influence the PRL releasing effect of domperidone in MBH-lesioned animals. The PRL stimulatory effect of domperidone (0.3 mg/kg, IV) in MBH-lesioned rats was antagonized by dopamine (20 μg/kg, IV) and bromocryptine (20 μg/kg, IV). The above results suggest that the stimulatory effect of domperidone on the pituitary PRL secretion is mediated-at least in part-through the pituitary D2 dopamine receptors, but not by the displacement of endogenous dopamine originating from the MBH and reaching the pituitary via portal vessels.

Original languageEnglish
Pages (from-to)151-154
Number of pages4
JournalBrain Research Bulletin
Volume44
Issue number2
DOIs
Publication statusPublished - 1997

Fingerprint

Domperidone
Prolactin
Hypothalamus
Haloperidol
Dopamine
Dopamine Antagonists
Injections
Bromocriptine
Dopamine D2 Receptors

Keywords

  • Dopamine
  • Doperidone
  • Haloperidol
  • Mediobasal hypothalamic lesion
  • Prolactin

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Domperidone stimulates prolactin secretion in rats with complete destruction of the mediobasal hypothalamus. / Kiem, D. T.; Nagy, Gy M.; Barna, I.; Makara, G.

In: Brain Research Bulletin, Vol. 44, No. 2, 1997, p. 151-154.

Research output: Contribution to journalArticle

@article{a0507a0c9c274413ba456ac62eb3bff0,
title = "Domperidone stimulates prolactin secretion in rats with complete destruction of the mediobasal hypothalamus",
abstract = "The main objective of this study was to further elucidate the functional relationship between endogenous dopamine and the prolactin (PRL)-releasing effect of the dopamine antagonists domperidone and haloperidol. We studied the effect of the above dopamine antagonists on the PRL secretion in control and mediobasal hypothalamus (MBH)-lesioned rats. Significant increase in basal plasma PRL levels was detected 7 days after complete surgical destruction of the MBH. Haloperidol injection (0.5 mg/kg, IV) was followed by an increased plasma PRL concentration in the sham-operated animals; however, in the MBH-lesioned rats where the basal PRL levels were high haloperidol failed to produce additional PRL release. In contrast to haloperidol, domperidone (0.1 mg/kg, IV) was able to further elevate the MBH-lesion induced high plasma PRL concentration. Moreover, the change in plasma PRL levels of the MBH-lesioned rats was parallel with that in the sham-lesioned animals after domperidone injections. When haloperidol was given prior to the domperidone injection it did not influence the PRL releasing effect of domperidone in MBH-lesioned animals. The PRL stimulatory effect of domperidone (0.3 mg/kg, IV) in MBH-lesioned rats was antagonized by dopamine (20 μg/kg, IV) and bromocryptine (20 μg/kg, IV). The above results suggest that the stimulatory effect of domperidone on the pituitary PRL secretion is mediated-at least in part-through the pituitary D2 dopamine receptors, but not by the displacement of endogenous dopamine originating from the MBH and reaching the pituitary via portal vessels.",
keywords = "Dopamine, Doperidone, Haloperidol, Mediobasal hypothalamic lesion, Prolactin",
author = "Kiem, {D. T.} and Nagy, {Gy M.} and I. Barna and G. Makara",
year = "1997",
doi = "10.1016/S0361-9230(97)00099-3",
language = "English",
volume = "44",
pages = "151--154",
journal = "Brain Research Bulletin",
issn = "0361-9230",
publisher = "Elsevier Inc.",
number = "2",

}

TY - JOUR

T1 - Domperidone stimulates prolactin secretion in rats with complete destruction of the mediobasal hypothalamus

AU - Kiem, D. T.

AU - Nagy, Gy M.

AU - Barna, I.

AU - Makara, G.

PY - 1997

Y1 - 1997

N2 - The main objective of this study was to further elucidate the functional relationship between endogenous dopamine and the prolactin (PRL)-releasing effect of the dopamine antagonists domperidone and haloperidol. We studied the effect of the above dopamine antagonists on the PRL secretion in control and mediobasal hypothalamus (MBH)-lesioned rats. Significant increase in basal plasma PRL levels was detected 7 days after complete surgical destruction of the MBH. Haloperidol injection (0.5 mg/kg, IV) was followed by an increased plasma PRL concentration in the sham-operated animals; however, in the MBH-lesioned rats where the basal PRL levels were high haloperidol failed to produce additional PRL release. In contrast to haloperidol, domperidone (0.1 mg/kg, IV) was able to further elevate the MBH-lesion induced high plasma PRL concentration. Moreover, the change in plasma PRL levels of the MBH-lesioned rats was parallel with that in the sham-lesioned animals after domperidone injections. When haloperidol was given prior to the domperidone injection it did not influence the PRL releasing effect of domperidone in MBH-lesioned animals. The PRL stimulatory effect of domperidone (0.3 mg/kg, IV) in MBH-lesioned rats was antagonized by dopamine (20 μg/kg, IV) and bromocryptine (20 μg/kg, IV). The above results suggest that the stimulatory effect of domperidone on the pituitary PRL secretion is mediated-at least in part-through the pituitary D2 dopamine receptors, but not by the displacement of endogenous dopamine originating from the MBH and reaching the pituitary via portal vessels.

AB - The main objective of this study was to further elucidate the functional relationship between endogenous dopamine and the prolactin (PRL)-releasing effect of the dopamine antagonists domperidone and haloperidol. We studied the effect of the above dopamine antagonists on the PRL secretion in control and mediobasal hypothalamus (MBH)-lesioned rats. Significant increase in basal plasma PRL levels was detected 7 days after complete surgical destruction of the MBH. Haloperidol injection (0.5 mg/kg, IV) was followed by an increased plasma PRL concentration in the sham-operated animals; however, in the MBH-lesioned rats where the basal PRL levels were high haloperidol failed to produce additional PRL release. In contrast to haloperidol, domperidone (0.1 mg/kg, IV) was able to further elevate the MBH-lesion induced high plasma PRL concentration. Moreover, the change in plasma PRL levels of the MBH-lesioned rats was parallel with that in the sham-lesioned animals after domperidone injections. When haloperidol was given prior to the domperidone injection it did not influence the PRL releasing effect of domperidone in MBH-lesioned animals. The PRL stimulatory effect of domperidone (0.3 mg/kg, IV) in MBH-lesioned rats was antagonized by dopamine (20 μg/kg, IV) and bromocryptine (20 μg/kg, IV). The above results suggest that the stimulatory effect of domperidone on the pituitary PRL secretion is mediated-at least in part-through the pituitary D2 dopamine receptors, but not by the displacement of endogenous dopamine originating from the MBH and reaching the pituitary via portal vessels.

KW - Dopamine

KW - Doperidone

KW - Haloperidol

KW - Mediobasal hypothalamic lesion

KW - Prolactin

UR - http://www.scopus.com/inward/record.url?scp=0030770090&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030770090&partnerID=8YFLogxK

U2 - 10.1016/S0361-9230(97)00099-3

DO - 10.1016/S0361-9230(97)00099-3

M3 - Article

VL - 44

SP - 151

EP - 154

JO - Brain Research Bulletin

JF - Brain Research Bulletin

SN - 0361-9230

IS - 2

ER -