PMID- 21554573
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20121002
LR  - 20110510
IS  - 0953-8194 (Print)
IS  - 0953-8194 (Linking)
VI  - 4
IP  - 1
DP  - 1992 Feb
TI  - Effects of Cyclic AMP and Andre-gens on in vitro Brain Aromatase Enzyme Activity 
      During Prenatal Development in the Rat.
PG  - 29-36
LID - 10.1111/j.1365-2826.1992.tb00341.x [doi]
AB  - In the rat, there is a marked but transient increase in hypothalamic aromatase 
      activity during the last week of fetal life. The present study was undertaken to 
      gain insight into the regulation of this developmental pattern. Hypothalamic 
      fragments comprising the medial basal hypothalamus and the suprachiasmatic region 
      (henceforth referred to as preoptic area) were explanted and cultured in 
      serum-free medium for 2 to 5 days. Aromatase activity was measured by the 
      formation of (3) H(2) O, utilizing either [1ss-(3) H]androstene-dione or [1ss-(3) 
      H]testosterone as substrate. Maximal rates of activity were obtained at a 
      saturating concentration of 0.3 muM [1ss-(3) H]testosterone. Confirmation of the 
      identity of the [(3) H]estradiol formed was demonstrated by recrystallization of 
      the derivatized estradiol to constant specific activity following incubation with 
      [1,2,6,7-(3) H]testosterone. In agreement with previous reports, in vivo 
      hypothalamic aromatase activity was negligible before gestational day (GD) 16, 
      increased strikingly by GD19 (>5.0 pmol/h/mg protein) and decreased, thereafter, 
      to low levels at GD22 ( approximately 1.0 pmol/h/mg protein). Medial basal 
      hypothalamus-preoptic area fragments explanted before GD17 failed to develop 
      aromatase activity in vitro. If the tissue was explanted on GD17 or 18 (i.e. when 
      the in vivo rate of activity was increasing), the enzyme activity did not 
      continue to increase, but it was rather maintained for 2 days before decreasing 
      in a manner that closely mimicked the decline observed in vivo. A similar, 
      butimmediate decline was observed when the tissue was explanted on GD19 (i.e. at 
      the time when theactivity peaks in vivo). Exposure of explants to either growth 
      factors (insulin-like growth factor II, epidermal growth factor, and basic or 
      acidic fibroblast growth factor), or steroids (estradiol-17ss, progesterone, 
      testosterone, dihydrotestosterone and corticosterone) failed to either increase 
      aromatase activity before the peak at GD19 or ameliorate its perinatal decline. 
      Increase of Ca(2+) fluxes with the ionophore A23187 or activation of the cyclic 
      AMP, cyclic GMP, or protein kinase C pathways were similarly ineffective, as was 
      angiotensin II, a recently proposed stimulator of neural aromatase. In contrast, 
      aromatase activity was suppressed 2- to 4-fold by activation of the cyclic AMP 
      pathway (with either forskolin or 8-bromo-cyclic AMP) or by the androgens, 
      testosterone and dihydrotestosterone. These results suggest that: 1) the 
      appearance of aromatase activity in the rat hypothalamus before GD17 requires the 
      unfolding of extrahypothalamic events, 2) the increase in aromatase activity that 
      occurs before GD19 also requires extrahypothalamic inputs and does not involve 
      any of the known intracellular signal transduction pathways, and 3) the decline 
      in activity observed after GD19 is regulated within the hypothalamus, and appears 
      to be determined, at least in part, by the activation of cyclic AMP formation. A 
      potential role for androgens is discussed.
FAU - Lephart, E D
AU  - Lephart ED
AD  - The Cecil H. and Ida Green Center for Reproductive Biology Sciences and The 
      Departments of Biochemistry and Obstetrics and Gynecology, The University of 
      Texas Southwestern Medical Center, 5323 Harry Mines Boulevard, Dallas, Texas 
      75235, USA. Division of Neuroscience, Oregon Regional Primate Research Center, 
      Beaverton, Oregon 97006, USA.
FAU - Simpson, E R
AU  - Simpson ER
FAU - Ojeda, S R
AU  - Ojeda SR
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Neuroendocrinol
JT  - Journal of neuroendocrinology
JID - 8913461
EDAT- 1992/02/01 00:00
MHDA- 1992/02/01 00:01
CRDT- 2011/05/11 06:00
PHST- 2011/05/11 06:00 [entrez]
PHST- 1992/02/01 00:00 [pubmed]
PHST- 1992/02/01 00:01 [medline]
AID - 10.1111/j.1365-2826.1992.tb00341.x [doi]
PST - ppublish
SO  - J Neuroendocrinol. 1992 Feb;4(1):29-36. doi: 10.1111/j.1365-2826.1992.tb00341.x.