PMID- 2019260
OWN - NLM
STAT- MEDLINE
DCOM- 19910524
LR  - 20181130
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 128
IP  - 5
DP  - 1991 May
TI  - Effects of N-methyl-D,L-aspartic acid on luteinizing hormone secretion in normal 
      mice and in hypogonadal mice with fetal preoptic area implants.
PG  - 2432-40
AB  - Many aspects of reproductive function are corrected in hypogonadal mice with 
      preoptic area grafts (HPG/POA). Gonadotropin release and gonadal development are 
      dependent on the presence of GnRH cells within the grafts and GnRH innervation of 
      the median eminence. This study examined the effect of a known modulator of GnRH 
      secretion, N-methyl-D,L-aspartic acid (NMA), in adult normal and HPG/POA male and 
      female mice. All HPG/POA males had significant testicular development after graft 
      surgery, and most HPG/POA females were in constant vaginal estrus and showed 
      ovarian and uterine development; a few also demonstrated ovulatory cyclicity 
      after pregnancies initiated by reflex ovulation. Groups of normal and HPG/POA 
      males that were intact (INT) or castrated (CX) 7 days before testing were 
      challenged with saline, NMA (20 mg/kg), and GnRH (100 ng/0.1 ml). Sequential 
      blood samples from awake animals were obtained via intracardiac catheters for 
      evaluation of plasma LH. There were significant increases in plasma LH after NMA 
      challenge in normal INT [n = 15; 0 min, 0.26 +/- 0.02 (mean +/- SE); 10 min, 1.20 
      +/- 0.10 ng/ml; P less than 0.05] and normal CX (n = 13; 0 min, 0.36 +/- 0.06, 10 
      min, 3.25 +/- 0.27). Plasma LH secretion in response to NMA was significantly 
      correlated (r = 0.786; P less than 0.001) with plasma LH release after the GnRH 
      challenge in normal males. In contrast, only 3 of 17 HPG/POA (1 INT and 2 CX) 
      showed increased circulating LH after NMA challenge, despite heightened pituitary 
      sensitivity to GnRH. Normal and HPG/POA female mice were ovariectomized (OX) or 
      OX and estrogen primed (OXE2) 7 days before testing. Intact cycling normal and 
      cycling HPG/POA mice were tested in estrus (EST). There was a greater response to 
      NMA in normal OX (n = 8; 0 min, 0.39 +/- 0.02; 10 min, 1.44 +/- 0.28) than in 
      OXE2 (n = 13; 0 min, 0.29 +/- 0.01; 10 min, 0.52 +/- 0.07) despite similar 
      gonadotroph sensitivity to GnRH. There was also a significant increase in plasma 
      LH in response to NMA in HPG/POA-OX (n = 7; 0 min, 0.50 +/- 0.10; 10 min, 1.62 
      +/- 0.22) and HPG/POA-OXE2 (n = 12; 0 min, 0.39 +/- 0.04; 10 min, 1.31 +/- 0.26). 
      Plasma LH levels after NMA treatment were significantly correlated with responses 
      to GnRH in female HPG/POA (r = 0.58; P less than 0.03), but not in normal 
      females. Neither normal-EST nor HPG/POA-EST had increased LH release after NMA 
      challenge, perhaps due to the low gonadotroph sensitivity in this state.(ABSTRACT 
      TRUNCATED AT 400 WORDS)
FAU - Saitoh, Y
AU  - Saitoh Y
AD  - Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029.
FAU - Silverman, A J
AU  - Silverman AJ
FAU - Gibson, M J
AU  - Gibson MJ
LA  - eng
GR  - HD-19077/HD/NICHD NIH HHS/United States
GR  - NS-20337/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Estrogens)
RN  - 33515-09-2 (Gonadotropin-Releasing Hormone)
RN  - 6384-92-5 (N-Methylaspartate)
RN  - 9002-67-9 (Luteinizing Hormone)
SB  - IM
MH  - Animals
MH  - Castration
MH  - Estrogens/pharmacology
MH  - Female
MH  - *Fetal Tissue Transplantation
MH  - Gonadotropin-Releasing Hormone/pharmacology
MH  - Gonads/pathology
MH  - Hypogonadism/*metabolism/pathology/physiopathology
MH  - Immunohistochemistry
MH  - Luteinizing Hormone/blood/*metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred Strains
MH  - N-Methylaspartate/*pharmacology
MH  - Organ Size
MH  - Preoptic Area/*embryology
MH  - Reference Values
EDAT- 1991/05/01 00:00
MHDA- 1991/05/01 00:01
CRDT- 1991/05/01 00:00
PHST- 1991/05/01 00:00 [pubmed]
PHST- 1991/05/01 00:01 [medline]
PHST- 1991/05/01 00:00 [entrez]
AID - 10.1210/endo-128-5-2432 [doi]
PST - ppublish
SO  - Endocrinology. 1991 May;128(5):2432-40. doi: 10.1210/endo-128-5-2432.