Inhibition of steroid-induced galanin mRNA expression in GnRH neurons by specific NMDA-receptor blockade

Winfried G. Rossmamth, Daniel Marks, Robert A. Steiner, Donald K. Clifton

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Galanin mRNA levels in GnRH neurons increase in association with a steroid-induced LH surge in female rats. Both the steroid-induced LH surge and the concomitant increase of galanin mRNA in GnRH neurons are blocked by non-specific inhibition of central nervous system activity imposed by pentobarbital and specific central alpha-adrenergic receptor blockade. Based on these observations, we hypothesized that galanin gene expression in GnRH neurons is induced whenever GnRH neurons become activated to generate an LH surge. If this were the case, then any neurotransmitter receptor blocking agent that inhibits the LH surge by central mechanisms would likewise block the associated increase in galanin mRNA in GnRH neurons. We tested this hypothesis by examining the effects of an N-methyl-D-aspartate (NMDA) receptor antagonist on the steroid-induced LH surge and on levels of galanin mRNA in GnRH neurons. Three groups of ovariectomized rats were used: Group 1-treated with estradiol and progesterone (E/P) and sacrificed at the peak of the LH surge; Group 2-treated the same as Group 1 except that dizocilpine (MK801, an NMDA receptor antagonist) was used to block the LH surge; and Group 3-treated the same as Group 1 except they received vehicle instead of E/P. Double-and single-label in situ hybridization followed by computerized image analysis were used to measure levels of galanin mRNA and GnRH mRNA in GnRH neurons [as grains/cell (g/c)]. E/P treatment induced a 3-fold increase in LH levels and a 5-fold increase in the galanin mRNA signal content of GnRH neurons. Treatment with MK801 completely prevented the LH surge in all animals and also blocked the steroid-induced increase in galanin mRNA in GnRH neurons. As assessed by 2 independent GnRH single-labeled assays, neither GnRH message content nor the number of identifiable GnRH neurons differed among the experimental groups. We conclude that the increase in galanin mRNA levels in GnRH neurons is tightly coupled to the occurrence of a steroid-evoked LH surge, and we infer that induction of galanin gene expression in GnRH neurons is induced as a consequence of synaptic activation of GnRH neurons.

Original languageEnglish (US)
Pages (from-to)179-184
Number of pages6
JournalJournal of Neuroendocrinology
Volume8
Issue number3
StatePublished - Mar 1996
Externally publishedYes

Fingerprint

Galanin
N-Methyl-D-Aspartate Receptors
Gonadotropin-Releasing Hormone
Steroids
Neurons
Messenger RNA
Progesterone
Estradiol
Gene Expression
Receptors, Adrenergic, alpha
Neurotransmitter Receptor
Dizocilpine Maleate
Pentobarbital

Keywords

  • Galanin
  • GnRH
  • In situ hybridization
  • LHRH
  • mRNA
  • NMDA

ASJC Scopus subject areas

  • Endocrinology
  • Neuroscience(all)

Cite this

Inhibition of steroid-induced galanin mRNA expression in GnRH neurons by specific NMDA-receptor blockade. / Rossmamth, Winfried G.; Marks, Daniel; Steiner, Robert A.; Clifton, Donald K.

In: Journal of Neuroendocrinology, Vol. 8, No. 3, 03.1996, p. 179-184.

Research output: Contribution to journalArticle

Rossmamth, Winfried G. ; Marks, Daniel ; Steiner, Robert A. ; Clifton, Donald K. / Inhibition of steroid-induced galanin mRNA expression in GnRH neurons by specific NMDA-receptor blockade. In: Journal of Neuroendocrinology. 1996 ; Vol. 8, No. 3. pp. 179-184.
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