1,721,119 research outputs found
TESTOSTERONE BINDING-PROTEIN IN THE ENCEPHALON AND PLASMA SEX-HORMONES DURING THE ANNUAL CYCLE IN RANA-ESCULENTA COMPLEX (AMPHIBIA-RANIDAE)
No full textTESTOSTERONE BINDING-PROTEIN IN THE ENCEPHALON AND PLASMA SEX-HORMONES DURING THE ANNUAL CYCLE IN RANA-ESCULENTA COMPLEX (AMPHIBIA-RANIDAE
In vivo and in vitro studies on effects of beta-endorphin and naloxone on sex steroids in the water frog, Rana esculenta.
No full textThe effects of beta-endorphin and its receptor antagonist, naloxone, on progesterone, androgens, and oestradiol-17 beta release in male and female Rana esculenta were studied in vivo and in vitro. In the in vivo experiments the frogs underwent hypophysectomy, gonadectomy or both, or were left intact; the animals were injected with beta-endorphin or naloxone and killed after 15, 30, 90 and 240 min. In the in vitro experiments inter-renal, testis and ovary, all with and without added pituitary, were incubated with beta-endorphin or naloxone for 10, 20, 40 and 80 min. The in vivo and in vitro data from males and females were in agreement. In vivo beta-endorphin increased progesterone in all experimental groups and oestradiol in intact and hypophysectomized frogs, while it decreased androgens in all experimental groups. In vitro beta-endorphin increased progesterone in inter-renal and gonadal tissue, and oestradiol in gonads only, while it decreased androgens in inter-renals and gonads. In vivo and in vitro naloxone induced opposite effects to beta-endorphin. These data suggest that in Rana esculenta, opioids are involved in the modulation of hypothalamo-pituitary-inter-renal and gonadal axes. In particular, the data indicate a direct effect of opioids on inter-renal and gonadal sex steroid production
In vivo and in vitro studies on the effects of mGnRH on oestradiol-17 beta inter-renal production in the female frog, Rana esculenta, during the post-reproductive period.
No full textPlasma oestradiol-17 beta was measured by RIA, in female, Rana esculenta, submitted to hypophysectomy, gonadectomy, or both, and treated with mammalian gonadotropin-releasing hormone (mGnRH), homologous pituitary homogenate, or both, during the post-reproductive period. In addition, the oestradiol-17 beta release was measured in in vitro incubations of ovaries or interrenals treated with mGnRH, pituitary, or both, during the same period. In vivo and in vitro mGnRH and/or pituitary directly stimulated the production of oestradiol-17 beta by the interrenal, but not by ovary, although the stimulatory effects of the pituitary are minor and delayed with respect to those of mGnRH. These results seem to indicate that mGnRH and pituitary, with probably different mechanisms, stimulate the interrenal to produce high levels of oestradiol which is involved in the post-reproductive refractorines
POSSIBLE ROLE OF ESTRADIOL-17-BETA DURING POSTREPRODUCTIVE PERIOD IN THE GREEN FROG, RANA-ESCULENTA COMPLEX
No full textPOSSIBLE ROLE OF ESTRADIOL-17-BETA DURING POSTREPRODUCTIVE PERIOD IN THE GREEN FROG, RANA-ESCULENTA COMPLE
Androgen synthesis modulation by prostaglandin E2 is differentially mediated via adenylate cyclase and phospholipase C in the testis of the crested newt, Triturus carnifex: in vitro studies.
No full textTo study the possible postreceptor mechanisms of prostaglandin E2 in modulating the male newt Triturus carnifex androgen synthesis, during reproduction, testes were in vitro superfused with medium alone, prostaglandin E2, protein kinase C activator (phorbol-12-myristate-13-acetate), prostaglandin E2 plus protein kinase C inhibitor (staurosporine), prostaglandin E2 plus phospholipase C inhibitor (compound 48/80), cAMP analog (dibutyryl cAMP), adenylate cyclase activator (forskolin), prostaglandin E2 plus AC inhibitor (2-0-methyladenosine), prostaglandin E2 plus protein kinase A inhibitor (H-89). In January (reproduction beginning), prostaglandin E2 and phorbol-12-myristate-13-acetate increased androgens, while staurosporine and compound 48/80 counteracted the prostaglandin E2 effect. In March (reproduction ending), prostaglandin E2, dibutyryl cAMP and forskolin decreased androgens, while 2-0-methyladenosine and H-89 counteracted the prostaglandin E2 effect. These data suggest that in Triturus carnifex prostaglandin E2 increases testicular androgens synthesis via phospholipase C at reproduction beginning; on the contrary, this prostaglandin decreases androgens via adenylate cyclase at reproduction ending
A novel neuropeptide cellular mechanism in amphibian interrenal steroidogenesis.
No full textInterrenals of female Rana esculenta were incubated with gonadotropin-releasing hormone (GnRH), 9-ketoreductase inhibitor (palmitic acid), acetyl salicyclic acid, prostaglandin F2 alpha (PGF2 alpha), forskolin, isobutylmethyl xanthine (IBMX), dibutyril cyclic adenosine monophosphate (dbcAMP). Prostaglandin E2 (PGE2), PGF2 alpha, testosterone and 17 beta-estradiol were assessed on the incubation media. In addition, in the same interrenals, 9-ketoreductase and aromatase activities were evaluated. GnRH increased PGF2 alpha, 17 beta-estradiol, 9-ketoreductase and aromatase, and decreased PGE2 and testosterone. PGF2 alpha increased 17 beta-estradiol and aromatase, and decreased testosterone. Palmitic acid counteracted GnRH effects, while forskolin, IBMX and dbcAMP showed the same PGF2 alpha effects. These results suggest that GnRH stimulates 9-ketoreductase enhancing PGF2 alpha which in turn activates aromatase through cAMP mediation in the interrenal of Rana esculenta
Prostaglandin E2 and prostaglandin F2 alpha involvement in the corticosterone and cortisol release by the female frog, Rana esculenta, during ovulation.
No full textInterrenal and ovarian tissues of Rana esculenta were incubated in vitro during the preovulatory, ovulatory and postovulatory phases to study the basal release of prostaglandin E2 (PGE2), prostaglandin F2alpha (PGF2alpha), corticosterone, and cortisol. The effects of exogenous PGE2 and PGF2alpha on interrenal and ovarian corticosteroid release were also studied. In addition, the plasma values of these four hormones were assessed during the same phases. During in vitro interrenal incubations, PGE2, PGF2alpha, corticosterone, and cortisol basal releases were higher in the postovulatory phase, PGE2 and PGF2alpha treatment in vitro increased corticosteroids during the ovulatory phase. During in vitro ovarian incubations, PGE2 basal release was higher in the preovulatory phase and PGF2alpha and corticosteroids in the ovulatory phase; PGE2 treatment in vitro decreased corticosteroids in the ovulatory phase, and PGF2alpha increased corticosteroids in the preovulatory and postovulatory phases. PGE2, corticosterone and cortisol plasma values were higher during the postovulatory phase, while PGF2alpha was elevated during the ovulatory phase. These findings suggest that ovarian corticosteroids could be considered one of the factors inducing ovulation and that their synthesis may be modified by PGs
In-vivo stimulatory effects of mammalian gonadotropin-releasing hormone in female frog, Rana esculenta, during the recovery phase.
No full textWe studied the effects of GnRH on plasma levels of androgens and 17beta-oestradiol in female Rana esculenta during the recovery phas
La communication hormonale du triton
No full textL'étrange cour du male de triton crété illustre la manière dont l'activité hormonale commande l'activité cérébrale et le comportement sexxue
Pituitary adenylate cyclase-activating polypeptide induces testicular testosterone synthesis through PGE2 mediation in crested newt, Triturus carnifex
No full textThe aim of the present work was to study the possible role of adenylate cyclase-activating polypeptide (PACAP) 38 in the testicular intracellular mechanism regulating steroidogenesis of crested newt, Triturus carnifex. Gonads were incubated in vitro with PACAP 38 and prostaglandin (PG) E2 alone or with inhibitors of cyclooxygenase (COX), adenylate cyclase (AC), and phospholipase C (PLC) for 30 min and 60 min. PGE2, PGF2α, testosterone, and estradiol-17β were measured in the culture medium; aromatase (AR) activity and cAMP were assessed in the tissue. PACAP 38 increased PGE2 (30 min and 60 min), estradiol-17β (60 min), cAMP (60 min), and AR (60 min) but decreased testosterone (60 min). PGE2 increased estradiol-17β, cAMP, and AR and decreased testosterone at 30 and 60 min.PLC inhibitor counteracted the effects of PACAP 38, while AC inhibitor counteracted these effects except for PGE2 increase. AC inhibitor counteracted the effects of PGE2, while PLC did not. COX inhibitor decreased PGF2α (30 min and 60 min), PGE2 (30 min and 60 min), estradiol-17β (60 min), cAMP (60 min), and AR (60 min), but increased testosterone (60 min). These in vitro results suggest that, in newt testis, PACAP 38 acts on PLC, inducing the increase of PGE2 which, in turn, acting on AC, increases AR activity with the consequent estradiol-17β increase and testosterone decrease
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