PMID- 8159277
OWN - NLM
STAT- MEDLINE
DCOM- 19940519
LR  - 20180214
IS  - 0028-3835 (Print)
IS  - 0028-3835 (Linking)
VI  - 59
IP  - 3
DP  - 1994 Mar
TI  - Opioidergic modulation of N-methyl-D,L-aspartic-acid-stimulated LH release in 
      young adult but not older male mice.
PG  - 277-84
AB  - Among the neuromodulators of the GnRH neuronal system are the endogenous opioid 
      peptides and the excitatory amino acids. Although the opioid antagonist naloxone 
      (NAL) induces LH secretion in many species, there are no reports of an effect of 
      NAL on LH release in mice. Our previous studies demonstrated that the excitatory 
      amino acid analog N-methyl-D,L-aspartic acid (NMA) stimulates LH release in mice 
      and suggested that NMA-induced LH release is mediated via afferents to GnRH 
      neurons. In the current study, the role of the endogenous opioid system in the 
      regulation of LH release in adult male mice was assessed by testing whether this 
      system is a component of the NMA-stimulated LH response. NAL, its quaternary 
      derivative NAL methiodide (which remains outside of the blood-brain barrier) and 
      saline (SAL) were administered alone and in combination with NMA via intravenous 
      catheters. Although neither opioid antagonist stimulated LH release when 
      administered alone, each significantly potentiated the LH response to NMA in 
      young adult (10- to 14-week-old) male mice (p < 0.01) but not in older (10- to 
      16-month-old) male mice. The equivalent action of the two ipioid blockers 
      suggested an action outside of the blood-brain barrier. To determine whether 
      opioid blockade altered pituitary sensitivity to GnRH, a dose response for 
      exogenously administered GnRH was first determined, and low and high doses of 
      GnRH were tested in combination with NAL or SAL. Neither treatment was effective 
      in altering the LH response to GnRH, indicating that the action of the opioid 
      antagonists was at a suprapituitary location. (ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Miller, G M
AU  - Miller GM
AD  - Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029.
FAU - Gibson, M J
AU  - Gibson MJ
LA  - eng
GR  - NS20335/NS/NINDS NIH HHS/United States
GR  - T32DK07645/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Switzerland
TA  - Neuroendocrinology
JT  - Neuroendocrinology
JID - 0035665
RN  - 0 (Endorphins)
RN  - 33515-09-2 (Gonadotropin-Releasing Hormone)
RN  - 36B82AMQ7N (Naloxone)
RN  - 6384-92-5 (N-Methylaspartate)
RN  - 9002-67-9 (Luteinizing Hormone)
SB  - IM
MH  - Aging/*metabolism
MH  - Animals
MH  - Cardiac Catheterization
MH  - Dose-Response Relationship, Drug
MH  - Endorphins/*physiology
MH  - Gonadotropin-Releasing Hormone/pharmacology
MH  - Luteinizing Hormone/*metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C3H
MH  - N-Methylaspartate/*pharmacology
MH  - Naloxone/pharmacology
MH  - Radioimmunoassay
EDAT- 1994/03/01 00:00
MHDA- 1994/03/01 00:01
CRDT- 1994/03/01 00:00
PHST- 1994/03/01 00:00 [pubmed]
PHST- 1994/03/01 00:01 [medline]
PHST- 1994/03/01 00:00 [entrez]
AID - 10.1159/000126669 [doi]
PST - ppublish
SO  - Neuroendocrinology. 1994 Mar;59(3):277-84. doi: 10.1159/000126669.