PMID- 19880810
OWN - NLM
STAT- MEDLINE
DCOM- 20100222
LR  - 20211020
IS  - 1945-7170 (Electronic)
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 151
IP  - 1
DP  - 2010 Jan
TI  - The kisspeptin/neurokinin B/dynorphin (KNDy) cell population of the arcuate 
      nucleus: sex differences and effects of prenatal testosterone in sheep.
PG  - 301-11
LID - 10.1210/en.2009-0541 [doi]
AB  - Recent work in sheep has identified a neuronal subpopulation in the arcuate 
      nucleus that coexpresses kisspeptin, neurokinin B, and dynorphin (referred to 
      here as KNDy cells) and that mediate the negative feedback influence of 
      progesterone on GnRH secretion. We hypothesized that sex differences in 
      progesterone negative feedback are due to sexual dimorphism of KNDy cells and 
      compared neuropeptide and progesterone receptor immunoreactivity in this 
      subpopulation between male and female sheep. In addition, because sex differences 
      in progesterone negative feedback and neurokinin B are due to the influence of 
      testosterone (T) during fetal life, we determined whether prenatal T exposure 
      would mimic sex differences in KNDy cells. Adult rams had nearly half the number 
      of kisspeptin, neurokinin B, dynorphin, and progesterone receptor-positive cells 
      in the arcuate nucleus as did females, but the percentage of KNDy cells 
      colocalizing progesterone receptors remained high in both sexes. Prenatal T 
      treatment also reduced the number of dynorphin, neurokinin B, and progesterone 
      receptor-positive cells in the female arcuate nucleus; however, the number of 
      kisspeptin cells remained high and at levels comparable to control females. Thus, 
      sex differences in kisspeptin in the arcuate nucleus, unlike that of dynorphin 
      and neurokinin B, are not due solely to exposure to prenatal T, suggesting the 
      existence of different critical periods for multiple peptides coexpressed within 
      the same neuron. In addition, the imbalance between inhibitory (dynorphin) and 
      stimulatory (kisspeptin) neuropeptides in this subpopulation provides a potential 
      explanation for the decreased ability of progesterone to inhibit GnRH neurons in 
      prenatal T-treated ewes.
FAU - Cheng, Guanliang
AU  - Cheng G
AD  - Department of Anatomy and Cell Biology, University of Western Ontario, London, 
      Ontario, Canada.
FAU - Coolen, Lique M
AU  - Coolen LM
FAU - Padmanabhan, Vasantha
AU  - Padmanabhan V
FAU - Goodman, Robert L
AU  - Goodman RL
FAU - Lehman, Michael N
AU  - Lehman MN
LA  - eng
GR  - R01 HD41098/HD/NICHD NIH HHS/United States
GR  - 86744/CAPMC/CIHR/Canada
GR  - R01 HD041098/HD/NICHD NIH HHS/United States
GR  - P01 HD44232/HD/NICHD NIH HHS/United States
GR  - R01 HD39916/HD/NICHD NIH HHS/United States
GR  - P01 HD044232/HD/NICHD NIH HHS/United States
GR  - R01 HD039916/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20091030
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (KISS1 protein, human)
RN  - 0 (Kisspeptins)
RN  - 0 (Oligopeptides)
RN  - 33515-09-2 (Gonadotropin-Releasing Hormone)
RN  - 3XMK78S47O (Testosterone)
RN  - 74913-18-1 (Dynorphins)
RN  - 86933-75-7 (Neurokinin B)
RN  - 9002-67-9 (Luteinizing Hormone)
SB  - IM
MH  - Animals
MH  - Arcuate Nucleus of Hypothalamus/cytology/drug effects/*metabolism
MH  - Dynorphins/*metabolism
MH  - Female
MH  - Gonadotropin-Releasing Hormone/metabolism
MH  - Kisspeptins
MH  - Luteinizing Hormone/blood
MH  - Male
MH  - Neurokinin B/*metabolism
MH  - Neurons/drug effects/metabolism
MH  - Oligopeptides/*metabolism
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects/blood/metabolism
MH  - Sex Characteristics
MH  - Sheep
MH  - Testosterone/*pharmacology
PMC - PMC2803147
EDAT- 2009/11/03 06:00
MHDA- 2010/02/23 06:00
PMCR- 2011/01/01
CRDT- 2009/11/03 06:00
PHST- 2009/11/03 06:00 [entrez]
PHST- 2009/11/03 06:00 [pubmed]
PHST- 2010/02/23 06:00 [medline]
PHST- 2011/01/01 00:00 [pmc-release]
AID - en.2009-0541 [pii]
AID - 5118 [pii]
AID - 10.1210/en.2009-0541 [doi]
PST - ppublish
SO  - Endocrinology. 2010 Jan;151(1):301-11. doi: 10.1210/en.2009-0541. Epub 2009 Oct 
      30.