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Noradrenergic Neurotoxin Suppresses Gonadotropin‐Releasing Hormone (GnRH) and GnRH Receptor Gene Expression in Ovariectomized and Steroid‐Treated Rats
Author(s) -
Kang Ss,
Son Gh,
Seong Jy,
Da-Hye Choi,
Kwon Hb,
Lee Cc,
Kim K
Publication year - 1998
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1046/j.1365-2826.1998.00278.x
Subject(s) - medicine , endocrinology , ovariectomized rat , luteinizing hormone , neurotoxin , gonadotropin releasing hormone , gonadotropin , preoptic area , neurotransmission , hypothalamus , biology , receptor , chemistry , hormone
The present study was designed to investigate whether noradrenergic neurotransmission regulates the gene expression of gonadotropin‐releasing hormone (GnRH) in the preoptic area and GnRH receptor in the pituitary. To this end, N‐(2‐chloroethyl)‐N‐ethyl‐2‐bromobenzylamine (DSP4, 50 mg/kg), an intraperitoneal (i.p.) injection of selective noradrenergic neurotoxin, was administered 1 h before progesterone (1 mg) treatment in ovariectomized and estradiol‐treated prepubertal rats. Treatment with DSP4 effectively blocked the progesterone‐induced increase in hypothalamic noradrenaline content, but not dopamine content, indicating that DSP4 selectively inhibits noradrenergic neurotransmission. DSP4 significantly blocked progesterone‐induced increase in serum luteinizing hormone (LH) concentrations as well as GnRH release from hypothalamic fragments incubated in vitro . DSP4 concomitantly down‐regulated GnRH mRNA levels in the preoptic area, as determined by competitive reverse transcription‐polymerase chain reaction. DSP4 also clearly down‐regulated progesterone‐induced GnRH receptor mRNA levels in the pituitary, whereas it failed to alter LH β mRNA levels. In summary, blockade of noradrenergic neurotransmission with DSP4 resulted in profound reductions of hypothalamic GnRH and pituitary GnRH receptor gene expression.