Alpha-1a-adrenergic Receptor OKDB#: 2809
 Symbols: ADRA1A Species: human
 Synonyms: ALPHA-1C-ADRENERGIC RECEPTOR, FORMERLY, ADRA1C, FORMERLY  Locus: 8p21 in Homo sapiens
HPMR


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General Comment
General function Receptor
Comment
Cellular localization Plasma membrane
Comment
Ovarian function
Comment The influence of alpha-adrenergic receptors stimulator and blockers and beta-blocker on the ovary and endocrinological activity in heifers during superovulation. Gajewski Z et al. Twenty five Holstein-Friesian heifers, clinically normal and with regular oestrous cycles, were used for induction of superovulation (PMSG-PGF(2)alpha-Neutra-PMSG). Animals were divided into 5 groups receiving: I - detomidine (40 mug/kg b.w.), II - doxazosin (0.2 mg/kg b.w.), III - yohimbine HCL 1% (1 ml/50 kg b.w.), IV - carazolol (0.01 mg/ kg b.w., i.v.), and V - physiological saline (1 ml/50 kg b.w.). The heifers with PGF2alpha-induced cycles were treated with the substances 88 hrs after being given a single i.m. injection of 2500 IU PMSG. All animals were examined by ultrasonography, and by the number and size of ovarian follicles > 3 mm in diameter. The follicles were divided into 3 groups according to the diameter. Blood plasma was stored at -20 degrees C until LH, P4, E2 and PGFM analyses. In the control (V) group, two waves of follicle growth were observed. Yohimbine produced a significant blockage of ovulation. The mean number of corpora lutea in the group III was significantly lower than that in the control group (p< 0.02). No significant differences in the number of corpora lutea were observed between the groups I, II and III. The increase in E2 concentrations could be the response to the PMSG treatment with two waves of growth of large follicles before and after ovulation. Pulsatile LH release was altered by yohimbinum injection, however, the greater amplitude of pulses immediately following yohimbinum administration are suggestive of a positive influence of the alpha-2 adrenergic receptors antagonist. Yohimbinum administration did not affect plasma concentration of examined hormones. There was a difference between the plasma levels of LH after the doxazosin injection. Single injection of the stimulators and blockers of adrenergic receptors did not affect superovulatory response in terms of the numbers of CL, unruptured follicles and embryos recovered. The affectivity of artificial insemination was not significantly different between the control group and the detomidinum groups, while in the yohimbinum group it was significantly lower.
Expression regulated by
Comment
Ovarian localization Luteal cells, Stromal cells
Comment Ovarian expression of alpha (1)- and beta (2)-adrenoceptors and p75 neurotrophin receptors in rats with steroid-induced polycystic ovaries Manni L, et al . Polycystic ovary syndrome (PCOS) is the main cause of infertility in women. Despite extensive research aimed at identifying the pathogenetic mechanism underlying this condition, the aetiology of the disease is still unknown. Evidence from studies on women with PCOS and on an experimental rat polycystic ovary (PCO) model suggests that the sympathetic regulatory drive to the ovary may be unbalanced. The present study was designed to investigate this hypothesis. Accordingly, we used the well-defined rat PCO model, where PCO is induced by a single intramuscular (i.m.) injection of estradiol valerate (EV), and compared the model with oil-injected controls. We studied the ovarian expression of the alpha(1)- and beta(2)-adrenoceptors (ARs), the neurotrophin receptor p75 (p75(NTR)), and the sympathetic marker tyrosine hydroxylase (TH) at two time points: 30 and 60 days after EV injection. Our data demonstrate for the first time that all of the alpha(1)-AR subtypes are expressed in normal rat ovaries at both the mRNA and the protein levels. Furthermore, the expression of the alpha(1)-AR subtypes was differentially modulated in a time- and subtype-dependent manner in rats with EV-induced PCO. The ovaries in rats with steroid-induced PCO are characterised by an early overexpression of these molecules and p75(NTR), while the beta(2)-AR was downregulated. An increase in the expression of ovarian TH after EV injection was also detected, suggesting a structural and functional remodelling of ovarian sympathetic innervation in PCO rats. Our evidence strongly indicates that the role of the sympathetic nervous system is crucial in the pathogenesis of EV-induced PCO. Overall, our findings suggest that therapeutical approaches aimed at down-regulating the sympathetic tone to the ovary could be useful in the prevention and clinical treatment of PCOS.
Follicle stages
Comment alpha(1)-Adrenergic receptor in rat ovary: Presence and localization Itoh MT, et al . Noradrenaline modulates ovarian steroidogenesis, stimulates ovulation, and probably promotes follicular development in the ovary. It has been suggested that these effects of noradrenaline are mediated by alpha- and/or beta-adrenergic receptors (ARs) in the ovary. The purpose of the present study was to examine whether alpha(1)-AR is present in the rat ovary. In Western blotting, antibody against alpha(1)-ARs recognized a major protein in the ovary of adult (10-week-old) rats with a molecular weight of 80kDa, which is similar to that of the alpha(1B)-AR subtype. Immunohistochemistry using this antibody showed that alpha(1)-AR was detected at various sites in the ovary, including large antral follicle, germinal epithelium at the circumference of large antral follicle, corpus luteum, and interstitial tissue. These results confirm that the ovary contains alpha(1)-AR (probably alpha(1B)-subtype), and suggest that this receptor mediates some of the activities of noradrenaline in the regulation of ovarian functions. Furthermore, we found that alpha(1)-AR is present in oocyte of large antral follicle, suggesting that noradrenaline acts on oocyte via this receptor.
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created: 2005-04-01 00:40:38 by: Aaron J Hsueh, hsuehlab   email: aaron.hsueh@stanford.edu
home page: http://reprobio.stanford.edu/hsueh
last update: 2007-01-24 10:19:19 by: Aaron J Hsueh, hsuehlab   email: aaron.hsueh@stanford.edu



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