The δ-opioid signal transduction on the gonadotropin-releasing hormone release is eicosanoid dependent

Kyriaki Gerozissis, Ioannis Dragatsis, Christine Zioudrou

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

In static incubations, the K+ induced release of gonadotropin-releasing hormone (GnRH) and of prostaglandin (PG) E2, was 2-3 times higher in the isolated median eminence (ME) compared to the hypothalamic area containing the arcuate nucleus (ARN) plus the ME. The δ-opioid agonist DTLET, induced a parallel, dose-dependent reduction of GnRH and PGE2 release in the ARN plus ME. Both effects of DTLET were blocked by the δ-opioid antagonist Diallyl-G. In the isolated ME, DTLET reduced the secretion of PGE2 but enhanced the release of GnRH. In this area Diallyl-G had no effect on the PGE2 release but blocked the GnRH secretion. When the PGE2 production was blocked by indomethacin in the ARN plus ME preparation, DTLET increased the release of GnRH and induced the production of leukotrienes (LTs). On the other hand, DTLET decreased the release of both GnRH and PGE2 in the presence of nordihydroguaiaretic acid (NDGA), an inhibitor of the production of LTs. The above results suggest that: (a) the δ-opioid agonist DTLET modulates GnRH release differentially in the hypothalamic areas examined; and (b) the arachidonic acid metabolites are involved in the mode of action of DTLET on the release of GnRH in the ARN plus ME hypothalamic fragment.

Original languageEnglish (US)
Pages (from-to)219-224
Number of pages6
JournalBrain Research
Volume626
Issue number1-2
DOIs
StatePublished - Oct 29 1993

Fingerprint

Eicosanoids
Gonadotropin-Releasing Hormone
Median Eminence
Opioid Analgesics
Signal Transduction
Dinoprostone
Arcuate Nucleus of Hypothalamus
Leukotrienes
Masoprocol
Narcotic Antagonists
deltakephalin
Arachidonic Acid
Indomethacin

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

Cite this

The δ-opioid signal transduction on the gonadotropin-releasing hormone release is eicosanoid dependent. / Gerozissis, Kyriaki; Dragatsis, Ioannis; Zioudrou, Christine.

In: Brain Research, Vol. 626, No. 1-2, 29.10.1993, p. 219-224.

Research output: Contribution to journalArticle

@article{f83b3712a4b146fc978bd9534e6d6054,
title = "The δ-opioid signal transduction on the gonadotropin-releasing hormone release is eicosanoid dependent",
abstract = "In static incubations, the K+ induced release of gonadotropin-releasing hormone (GnRH) and of prostaglandin (PG) E2, was 2-3 times higher in the isolated median eminence (ME) compared to the hypothalamic area containing the arcuate nucleus (ARN) plus the ME. The δ-opioid agonist DTLET, induced a parallel, dose-dependent reduction of GnRH and PGE2 release in the ARN plus ME. Both effects of DTLET were blocked by the δ-opioid antagonist Diallyl-G. In the isolated ME, DTLET reduced the secretion of PGE2 but enhanced the release of GnRH. In this area Diallyl-G had no effect on the PGE2 release but blocked the GnRH secretion. When the PGE2 production was blocked by indomethacin in the ARN plus ME preparation, DTLET increased the release of GnRH and induced the production of leukotrienes (LTs). On the other hand, DTLET decreased the release of both GnRH and PGE2 in the presence of nordihydroguaiaretic acid (NDGA), an inhibitor of the production of LTs. The above results suggest that: (a) the δ-opioid agonist DTLET modulates GnRH release differentially in the hypothalamic areas examined; and (b) the arachidonic acid metabolites are involved in the mode of action of DTLET on the release of GnRH in the ARN plus ME hypothalamic fragment.",
author = "Kyriaki Gerozissis and Ioannis Dragatsis and Christine Zioudrou",
year = "1993",
month = "10",
day = "29",
doi = "10.1016/0006-8993(93)90582-8",
language = "English (US)",
volume = "626",
pages = "219--224",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "1-2",

}

TY - JOUR

T1 - The δ-opioid signal transduction on the gonadotropin-releasing hormone release is eicosanoid dependent

AU - Gerozissis, Kyriaki

AU - Dragatsis, Ioannis

AU - Zioudrou, Christine

PY - 1993/10/29

Y1 - 1993/10/29

N2 - In static incubations, the K+ induced release of gonadotropin-releasing hormone (GnRH) and of prostaglandin (PG) E2, was 2-3 times higher in the isolated median eminence (ME) compared to the hypothalamic area containing the arcuate nucleus (ARN) plus the ME. The δ-opioid agonist DTLET, induced a parallel, dose-dependent reduction of GnRH and PGE2 release in the ARN plus ME. Both effects of DTLET were blocked by the δ-opioid antagonist Diallyl-G. In the isolated ME, DTLET reduced the secretion of PGE2 but enhanced the release of GnRH. In this area Diallyl-G had no effect on the PGE2 release but blocked the GnRH secretion. When the PGE2 production was blocked by indomethacin in the ARN plus ME preparation, DTLET increased the release of GnRH and induced the production of leukotrienes (LTs). On the other hand, DTLET decreased the release of both GnRH and PGE2 in the presence of nordihydroguaiaretic acid (NDGA), an inhibitor of the production of LTs. The above results suggest that: (a) the δ-opioid agonist DTLET modulates GnRH release differentially in the hypothalamic areas examined; and (b) the arachidonic acid metabolites are involved in the mode of action of DTLET on the release of GnRH in the ARN plus ME hypothalamic fragment.

AB - In static incubations, the K+ induced release of gonadotropin-releasing hormone (GnRH) and of prostaglandin (PG) E2, was 2-3 times higher in the isolated median eminence (ME) compared to the hypothalamic area containing the arcuate nucleus (ARN) plus the ME. The δ-opioid agonist DTLET, induced a parallel, dose-dependent reduction of GnRH and PGE2 release in the ARN plus ME. Both effects of DTLET were blocked by the δ-opioid antagonist Diallyl-G. In the isolated ME, DTLET reduced the secretion of PGE2 but enhanced the release of GnRH. In this area Diallyl-G had no effect on the PGE2 release but blocked the GnRH secretion. When the PGE2 production was blocked by indomethacin in the ARN plus ME preparation, DTLET increased the release of GnRH and induced the production of leukotrienes (LTs). On the other hand, DTLET decreased the release of both GnRH and PGE2 in the presence of nordihydroguaiaretic acid (NDGA), an inhibitor of the production of LTs. The above results suggest that: (a) the δ-opioid agonist DTLET modulates GnRH release differentially in the hypothalamic areas examined; and (b) the arachidonic acid metabolites are involved in the mode of action of DTLET on the release of GnRH in the ARN plus ME hypothalamic fragment.

UR - http://www.scopus.com/inward/record.url?scp=0027374179&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027374179&partnerID=8YFLogxK

U2 - 10.1016/0006-8993(93)90582-8

DO - 10.1016/0006-8993(93)90582-8

M3 - Article

VL - 626

SP - 219

EP - 224

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1-2

ER -