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[PMID]:21377487
[Au] Autor:Henley CL; Nunez AA; Clemens LG
[Ad] Endereço:Departments of Zoology and Psychology, and the Neuroscience Program, Michigan State University, East Lansing, MI 48824, USA.
[Ti] Título:Hormones of choice: the neuroendocrinology of partner preference in animals.
[So] Source:Front Neuroendocrinol;32(2):146-54, 2011 Apr.
[Is] ISSN:1095-6808
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Partner preference behavior can be viewed as the outcome of a set of hierarchical choices made by an individual in anticipation of mating. The first choice involves approaching a conspecific verses an individual of another species. As a rule, a conspecific is picked as a mating partner, but early life experiences can alter that outcome. Within a species, an animal then has the choice between a member of the same sex or the opposite sex. The final choice is for a specific individual. This review will focus on the middle choice, the decision to mate with either a male or a female. Available data from rats, mice, and ferrets point to the importance of perinatal exposure to steroid hormones in the development of partner preferences, as well as the importance of activational effects in adulthood. However, the particular effects of this hormone exposure show species differences in both the specific steroid hormone responsible for the organization of behavior and the developmental period when it has its effect. Where these hormones have an effect in the brain is mostly unknown, but regions involved in olfaction and sexual behavior, as well as sexually dimorphic regions, seem to play a role. One limitation of the literature base is that many mate or 'partner preference studies' rely on preference for a specific stimulus (usually olfaction) but do not include an analysis of the relation, if any, that stimulus has to the choice of a particular sexual partner. A second limitation has been the almost total lack of attention to the type of behavior that is shown by the choosing animal once a 'partner' has been chosen, specifically, if the individual plays a mating role typical of its own sex or the opposite sex. Additional paradigms that address these questions are needed for better understanding of partner preferences in rodents.
[Mh] Termos MeSH primário: Comportamento de Escolha/fisiologia
Preferência de Acasalamento Animal
[Mh] Termos MeSH secundário: Androstatrienos/farmacologia
Animais
Castração
Comportamento de Escolha/efeitos dos fármacos
Feminino
Furões
Hormônios
Masculino
Camundongos
Nitromifeno/farmacologia
Ligação do Par
Gravidez
Efeitos Tardios da Exposição Pré-Natal
Área Pré-Óptica/efeitos dos fármacos
Área Pré-Óptica/fisiologia
Ratos
Caracteres Sexuais
Olfato
Testosterona/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (1,4,6-androstatrien-3,17-dione); 0 (Androstatrienes); 0 (Hormones); 3XMK78S47O (Testosterone); 5FS1NJ6Q8N (Nitromifene)
[Em] Mês de entrada:1108
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110308
[St] Status:MEDLINE
[do] DOI:10.1016/j.yfrne.2011.02.010


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[PMID]:16198490
[Au] Autor:Nakamura NH; McEwen BS
[Ad] Endereço:Laboratory of Neuroendocrinology, The Rockefeller University, Box 165, 1230 York Avenue, New York, NY 10021-6399, USA. nakamun@rockefeller.edu
[Ti] Título:Changes in interneuronal phenotypes regulated by estradiol in the adult rat hippocampus: a potential role for neuropeptide Y.
[So] Source:Neuroscience;136(1):357-69, 2005.
[Is] ISSN:0306-4522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ovarian hormones regulate pyramidal cell synapse formation and excitability and interneuronal GABAergic tone in the CA1 region of the adult female rat hippocampus. The role of 17beta-estradiol in these effects is complex and appears to involve a subset of hippocampal interneurons, which express different calcium-binding protein and neuropeptide phenotypes and nuclear estrogen receptor alpha. We found that, in the hippocampus, nuclear estrogen receptor alpha-immunoreactive interneurons co-express neuropeptide Y, calbindin-D28k and calretinin but do not parvalbumin or cholecystokinin. Moreover, a proportion of neuropeptide Y-immunoreactive interneurons co-expresses calbindin-D28k and calretinin. This pattern is similar in the presence or absence of 17beta-estradiol treatment in ovariectomized rats. We then used immunohistochemistry and in situ hybridization to determine whether 17beta-estradiol treatment regulates expression of CA1 interneuronal phenotypic markers via nuclear estrogen receptor alpha activation. We found that 17beta-estradiol treatment of ovariectomized rats increased neuropeptide Y mRNA levels (25%) and the neuropeptide Y mRNA-associated grain density per cell (11%), as well as the number of neuropeptide Y-immunoreactive cells (11%), predominantly in the pyramidal cell layer (stratum pyramidale). Treatment with CI628, a selective estrogen response modulator that acts as an antagonist for nuclear estrogen receptor, blocked 17beta-estradiol-induced increase of neuropeptide Y mRNA levels. 17beta-Estradiol treatment did not alter the number of parvalbumin, calretinin, and cholecystokinin immunoreactive cells, nor mRNA levels for parvalbumin and cholecystokinin. Therefore, the present study has identified neuropeptide Y expression as the main interneuronal phenotype that co-expresses nuclear estrogen receptor alpha and shown that neuropeptide Y is responsive to 17beta-estradiol in CA1 pyramidal cell layer. We suggest that 17beta-estradiol may regulate neuropeptide Y expression mediated by nuclear estrogen receptor alpha-dependent activation in a subset of hippocampal interneurons, and we speculate that subsequent neuropeptide Y release may indirectly contribute to regulate glutamate-dependent neuronal activity in the adult rat hippocampus.
[Mh] Termos MeSH primário: Estradiol/fisiologia
Hipocampo/fisiologia
Interneurônios/fisiologia
Neuropeptídeo Y/fisiologia
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Estradiol/sangue
Estradiol/farmacologia
Receptor alfa de Estrogênio/antagonistas & inibidores
Receptor alfa de Estrogênio/metabolismo
Feminino
Hipocampo/citologia
Imuno-Histoquímica
Hibridização In Situ
Neuropeptídeo Y/genética
Nitromifeno/farmacologia
Ovariectomia
Fenótipo
RNA Mensageiro/metabolismo
Ratos
Ratos Sprague-Dawley
Moduladores Seletivos de Receptor Estrogênico/farmacologia
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Biomarkers); 0 (Estrogen Receptor alpha); 0 (Neuropeptide Y); 0 (RNA, Messenger); 0 (Selective Estrogen Receptor Modulators); 4TI98Z838E (Estradiol); 5FS1NJ6Q8N (Nitromifene)
[Em] Mês de entrada:0602
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:051004
[St] Status:MEDLINE


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[PMID]:12488344
[Au] Autor:Rudick CN; Woolley CS
[Ad] Endereço:Department of Neurobiology and Physiology, Northwestern University, Evanston, Illinois 60208, USA.
[Ti] Título:Selective estrogen receptor modulators regulate phasic activation of hippocampal CA1 pyramidal cells by estrogen.
[So] Source:Endocrinology;144(1):179-87, 2003 Jan.
[Is] ISSN:0013-7227
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Previous studies demonstrated that estrogen induces two sequential waves of CA1 pyramidal cell activation, evidenced by induction of c-Fos at 2 and 24 h after a single estrogen treatment. The second wave of activation is paralleled by suppression of immunoreactivity for glutamic acid decarboxylase-65kD (GAD65) in CA1 and decreased synaptic inhibition of CA1 pyramidal cells. Here, we report that pretreatment with either of the selective estrogen receptor (ER) modulators, tamoxifen (T) or CI628, has no effect on the first wave of c-Fos expression at 2 h but completely blocks the second wave of c-Fos and the suppression of GAD65 at 24 h. Interestingly, T, given 4 h after estrogen, failed to block c-Fos expression or suppression of GAD65 at 24 h. Electrophysiological experiments showed that the T metabolite, 4OH-T, or CI628 can inhibit the so-called rapid estrogen effect, to potentiate excitatory postsynaptic currents (EPSCs) in CA1 pyramidal cells. Thus, estrogen seems to act within 4 h via classical ERs and/or a rapid estrogen effect, such as EPSC potentiation, to produce activation/disinhibition of pyramidal cells 24 h later. In contrast, the initial activation of pyramidal cells, at 2 h after estrogen, seems to involve neither classical ERs nor rapid potentiation of EPSCs.
[Mh] Termos MeSH primário: Estradiol/análogos & derivados
Estradiol/farmacologia
Células Piramidais/efeitos dos fármacos
Células Piramidais/fisiologia
Moduladores Seletivos de Receptor Estrogênico/farmacologia
Tamoxifeno/análogos & derivados
[Mh] Termos MeSH secundário: Animais
Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos
Feminino
Glutamato Descarboxilase/análise
Isoenzimas/análise
Cinética
Nitromifeno/farmacologia
Ovariectomia
Proteínas Proto-Oncogênicas c-fos/análise
Ratos
Tamoxifeno/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Isoenzymes); 0 (Proto-Oncogene Proteins c-fos); 0 (Selective Estrogen Receptor Modulators); 094ZI81Y45 (Tamoxifen); 17197F0KYM (afimoxifene); 1S4CJB5ZGN (estradiol 3-benzoate); 4TI98Z838E (Estradiol); 5FS1NJ6Q8N (Nitromifene); EC 4.1.1.15 (Glutamate Decarboxylase); EC 4.1.1.15 (glutamate decarboxylase 2)
[Em] Mês de entrada:0301
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:021219
[St] Status:MEDLINE


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[PMID]:11750181
[Au] Autor:Young EA; Altemus M; Parkison V; Shastry S
[Ad] Endereço:Department of Psychiatry and Mental Health Research Institute, University of Michigan, Ann Arbor, MI 48109-0729, USA. eayoung@umich.edu
[Ti] Título:Effects of estrogen antagonists and agonists on the ACTH response to restraint stress in female rats.
[So] Source:Neuropsychopharmacology;25(6):881-91, 2001 Dec.
[Is] ISSN:0893-133X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Previous studies have found that female rats are less sensitive than males to hypothalamic-pituitary-adrenal axis feedback inhibition by exogenous glucocorticoid administration. To determine whether estrogen contributes to this sex difference, we examined the effects of the estrogen antagonists tamoxifen and C1628 on the ACTH and corticosterone responses to restraint stress. CI628 increased both the ACTH and corticosterone response to restraint stress, and tamoxifen increased the ACTH response to restraint. Using overiectomized female rats, we also examined the effects of seven days of estradiol and/or progesterone replacement. Low dose estradiol decreased the ACTH but not the corticosterone response to restraint stress while progesterone had no effect on ACTH or corticosterone responses. The combination of estradiol and progesterone also decreased the ACTH response to stress, and the magnitude of the effect did not differ from that found with estradiol treatment alone. These data suggest that in the physiological range estradiol is an important inhibitory factor in the hypothalamic-pituitary-adrenal stress response of females.
[Mh] Termos MeSH primário: Hormônio Adrenocorticotrópico/metabolismo
Antagonistas de Estrogênios/farmacologia
Estrogênios/agonistas
Estresse Psicológico/metabolismo
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/administração & dosagem
Anti-Inflamatórios/farmacologia
Corticosterona/administração & dosagem
Corticosterona/farmacologia
Implantes de Medicamento/administração & dosagem
Implantes de Medicamento/farmacologia
Estradiol/farmacologia
Retroalimentação/efeitos dos fármacos
Feminino
Glucocorticoides/antagonistas & inibidores
Sistema Hipotálamo-Hipofisário/efeitos dos fármacos
Masculino
Nitromifeno/farmacologia
Ovariectomia
Progesterona/farmacologia
Ratos
Ratos Sprague-Dawley
Restrição Física
Tamoxifeno/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Drug Implants); 0 (Estrogen Antagonists); 0 (Estrogens); 0 (Glucocorticoids); 094ZI81Y45 (Tamoxifen); 4G7DS2Q64Y (Progesterone); 4TI98Z838E (Estradiol); 5FS1NJ6Q8N (Nitromifene); 9002-60-2 (Adrenocorticotropic Hormone); W980KJ009P (Corticosterone)
[Em] Mês de entrada:0201
[Cu] Atualização por classe:150311
[Lr] Data última revisão:
150311
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:011226
[St] Status:MEDLINE


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[PMID]:10067823
[Au] Autor:McEwen BS; Tanapat P; Weiland NG
[Ad] Endereço:Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, Rockefeller University, New York, New York 10021, USA. mcewen@rockvax.rockefeller.edu
[Ti] Título:Inhibition of dendritic spine induction on hippocampal CA1 pyramidal neurons by a nonsteroidal estrogen antagonist in female rats.
[So] Source:Endocrinology;140(3):1044-7, 1999 Mar.
[Is] ISSN:0013-7227
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Estrogens regulate the formation of excitatory synaptic connections in the hippocampus of female rats. Because the adult hippocampus has a very low concentration of intracellular estrogen receptors, it is unclear whether a conventional genomic mechanism is involved. Nonsteroidal estrogen antagonists are useful tools to study estrogen action because they can provide pharmacological data in favor of a particular pathway of estrogen action and evidence against other pathways. To investigate the role of intracellular estrogen receptors in the estrogen induction of synapse formation, we took advantage of previous studies in which we had shown that an estrogen antagonist, CI-628, enters the brain and blocks estrogen induction of progestin receptors to study whether the same antagonist would either mimic or block effects of estradiol to induce excitatory spine synapses. Using silver impregnation of neurons by the single section Golgi technique and morphometric analysis, we found that CI-628 effectively prevented estrogen induction of spines on CA1 pyramidal neurons, without having any agonist effects of its own. This result is consistent with an action of estradiol via intracellular estrogen receptors that are known to be expressed by interneurons within the hippocampus.
[Mh] Termos MeSH primário: Dendritos/efeitos dos fármacos
Antagonistas de Estrogênios/farmacologia
Nitromifeno/farmacologia
Células Piramidais/efeitos dos fármacos
Receptores Estrogênicos/fisiologia
[Mh] Termos MeSH secundário: Animais
Estradiol/farmacologia
Feminino
Células Piramidais/ultraestrutura
Ratos
Ratos Sprague-Dawley
Sinapses/fisiologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Estrogen Antagonists); 0 (Receptors, Estrogen); 4TI98Z838E (Estradiol); 5FS1NJ6Q8N (Nitromifene)
[Em] Mês de entrada:9903
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:990306
[St] Status:MEDLINE


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[PMID]:9887181
[Au] Autor:Kisley LR; Sakai RR; Ma LY; Fluharty SJ
[Ad] Endereço:Departments of Animal Biology and Pharmacology and the Institute of Neurological Sciences, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6046, USA.
[Ti] Título:Ovarian steroid regulation of angiotensin II-induced water intake in the rat.
[So] Source:Am J Physiol;276(1 Pt 2):R90-6, 1999 Jan.
[Is] ISSN:0002-9513
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Spontaneous water intake as well as thirst elicited by ANG II has been shown to be influenced by the stage of the estrous cycle in the female rat. In these experiments, the contribution of each of the ovarian steroid hormones to the regulation of water intake was examined. Ovariectomized female rats were given replacement doses of estrogen, progesterone, or both, and their responsiveness to an intracerebroventricular injection of ANG II was tested. Forty-eight-hour treatment with estradiol benzoate attenuated ANG II-induced thirst by as much as 70% compared with control animals. The effect of estrogen on drinking was dose dependent and could be completely blocked with concurrent administration of the antiestrogen CI-628. In contrast, progesterone, given alone or after estrogen, did not significantly affect ANG II-induced water intake when animals were tested at 4 or 24 h after steroid administration. A central interaction between the peptide hormone ANG II and estrogen, involving a genomic mechanism, may underlie the cyclicity in water intake behavior observed in the rat.
[Mh] Termos MeSH primário: Angiotensina II/farmacologia
Ingestão de Líquidos/efeitos dos fármacos
Estradiol/farmacologia
Progesterona/farmacologia
[Mh] Termos MeSH secundário: Animais
Carbacol/farmacologia
Relação Dose-Resposta a Droga
Antagonistas de Estrogênios/farmacologia
Feminino
Injeções Intraventriculares
Nitromifeno/farmacologia
Ratos
Ratos Sprague-Dawley
Sede/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Estrogen Antagonists); 11128-99-7 (Angiotensin II); 4G7DS2Q64Y (Progesterone); 4TI98Z838E (Estradiol); 5FS1NJ6Q8N (Nitromifene); 8Y164V895Y (Carbachol)
[Em] Mês de entrada:9903
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:990114
[St] Status:MEDLINE


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[PMID]:7557922
[Au] Autor:Vega Matuszczyk JV; Larsson K
[Ad] Endereço:Department of Psychology, University of Göteborg, Sweden.
[Ti] Título:Sexual preference and feminine and masculine sexual behavior of male rats prenatally exposed to antiandrogen or antiestrogen.
[So] Source:Horm Behav;29(2):191-206, 1995 Jun.
[Is] ISSN:0018-506X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Male rats were prenatally (Day 10-19 of pregnancy) exposed to an antiestrogen, nitromifene citrate (CI628, 1 mg/rat), or an antiandrogen, cyproterone acetate (CA, 10 mg/rat), and in adulthood were examined for their exhibition of male-typical and female-typical behavior pattern. Treatment with CI628 abolished the capacity of the adult intact male to ejaculate, enhanced his potential to exhibit feminine sexual behavior, and decreased the intensity of the level of female-oriented behavior in a two-choice stimulus situation (estrous female vs active male). The administration of testosterone (T) did not alter these behaviors. Males exposed to CA showed low levels of lordosis behavior and normal levels of female-oriented preference. Further, they showed increased frequency of mounts and decreased number of intromissions, and only a few males ever ejaculated. Macroscopic inspection of the genital organs of the CI628-treated males revealed complete absence of the prostate. The dissections of the CA-treated males revealed a poorly developed penis and a blind-ending vagina. It was concluded that prenatal estrogen (E) is involved (1) in determining the development of mechanisms destined to mediate the display of male-typical behaviors in adulthood, (2) in suppressing the development of mechanisms of female-typical behaviors, and (3) seems to stimulate neural mechanisms influencing sexual preference behavior in the adult.
[Mh] Termos MeSH primário: Antagonistas de Androgênios/farmacologia
Acetato de Ciproterona/farmacologia
Antagonistas de Estrogênios/farmacologia
Nitromifeno/farmacologia
Diferenciação Sexual/efeitos dos fármacos
Comportamento Sexual Animal/efeitos dos fármacos
Maturidade Sexual/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Copulação/efeitos dos fármacos
Ejaculação/efeitos dos fármacos
Feminino
Genitália Masculina/efeitos dos fármacos
Genitália Masculina/embriologia
Masculino
Gravidez
Efeitos Tardios da Exposição Pré-Natal
Ratos
Ratos Wistar
Testosterona/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Androgen Antagonists); 0 (Estrogen Antagonists); 3XMK78S47O (Testosterone); 4KM2BN5JHF (Cyproterone Acetate); 5FS1NJ6Q8N (Nitromifene)
[Em] Mês de entrada:9511
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:950601
[St] Status:MEDLINE


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[PMID]:1893270
[Au] Autor:Sayag N; Snapir N; Arnon E; el Halawani ME; Grimm VE; Robinzon B
[Ad] Endereço:Department of Animal Science, Faculty of Agriculture, Hebrew University of Jerusalem, Rehovot, Israel.
[Ti] Título:Sexual differentiation of copulatory behaviour in the male chick requires gonadal steroids.
[So] Source:Br Poult Sci;32(3):607-17, 1991 Jul.
[Is] ISSN:0007-1668
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:1. Embryonic injections of 0.3 mg/egg of tamoxifen (TAM), 0.2 mg/egg CI-628 (both antioestrogens), 0.5 mg/egg (ATD (aromatisation inhibitor), or antibodies to oestradiol (E), all suppressed male copulatory activity (MCA) in young male chicks. 2. Embryonic injections with either flutamide (F, androgen antagonist) or high dose of antibodies to testosterone (T) only slightly suppressed MCA. 3. TAM had no effect on embryonic plasma LH levels, 24 and 48 h after injection. 4. It seems that at the embryonic stage oestradiol is required for the normal differentiation of MCA.
[Mh] Termos MeSH primário: Embrião de Galinha/fisiologia
Estradiol/fisiologia
Diferenciação Sexual/fisiologia
Comportamento Sexual Animal/fisiologia
[Mh] Termos MeSH secundário: Animais
Inibidores da Aromatase
Embrião de Galinha/efeitos dos fármacos
Estradiol/imunologia
Feminino
Flutamida/farmacologia
Soros Imunes/imunologia
Hormônio Luteinizante/sangue
Masculino
Nitromifeno/farmacologia
Diferenciação Sexual/efeitos dos fármacos
Tamoxifeno/farmacologia
Testosterona/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aromatase Inhibitors); 0 (Immune Sera); 094ZI81Y45 (Tamoxifen); 3XMK78S47O (Testosterone); 4TI98Z838E (Estradiol); 5FS1NJ6Q8N (Nitromifene); 76W6J0943E (Flutamide); 9002-67-9 (Luteinizing Hormone)
[Em] Mês de entrada:9110
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:910701
[St] Status:MEDLINE


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[PMID]:2407900
[Au] Autor:Huet-Hudson YM; Dey SK
[Ad] Endereço:Department of Obstetrics/Gynecology and Physiology, University of Kansas Medical Center, Ralph L. Smith Research Center, Kansas City 66103.
[Ti] Título:Differential effects of ovarian steroids and triphenylethylene compounds on macromolecular uptake and thymidine incorporation in the mouse uterus.
[So] Source:J Steroid Biochem;35(1):23-7, 1990 Jan.
[Is] ISSN:0022-4731
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In the rodent uterus, estrogen elicits a biphasic response i.e. an early phase (Phase I) and a late phase (Phase II). Estradiol-17 beta (E2) and estriol (E3), as well as triphenylethylene (TPE) compounds, CI-628 and clomiphene citrate (CC), were used to characterize Phase I and Phase II responses in uterine preparation for implantation in the mouse. While uterine macromolecular uptake (vascular permeability), a Phase I response, was studied in progesterone (P4)-primed animals, uterine [3H]thymidine incorporation (DNA synthesis), a Phase II response, was investigated with and without P4-priming. In the P4-primed uterus, all compounds, except CC, significantly increased uterine macromolecular uptake as determined by interstitial tissue accumulation of [125I]bovine serum albumin [( 125I]BSA). DNA synthesis as determined by cellular incorporation of [3H]thymidine was modulated by P4, estrogens and TPE compounds in a cell-type specific and temporal manner. As a single injection and in the absence of P4, E2 induced [3H]thymidine incorporation in the luminal and glandular epithelium at 18 and 24 h. E3 was inferior to E2 in this response. On the other hand, treatment with P4 for 1 day or 4 days induced [3H]thymidine incorporation primarily in stromal cells. However, stromal cell incorporation was potentiated when P4 treatment was combined with estrogens or TPE compounds. These results reveal the relative importance of Phase I and cell-type specific Phase II responses in uterine preparation for implantation.
[Mh] Termos MeSH primário: Permeabilidade Capilar/efeitos dos fármacos
DNA/biossíntese
Estrogênios/farmacologia
Progesterona/farmacologia
Estilbenos/farmacologia
Útero/metabolismo
[Mh] Termos MeSH secundário: Animais
Clomifeno/farmacologia
Estradiol/farmacologia
Estriol/farmacologia
Feminino
Camundongos
Nitromifeno/farmacologia
Soroalbumina Bovina/metabolismo
Útero/irrigação sanguínea
Útero/efeitos dos fármacos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Estrogens); 0 (Stilbenes); 1HRS458QU2 (Clomiphene); 27432CM55Q (Serum Albumin, Bovine); 4G7DS2Q64Y (Progesterone); 4TI98Z838E (Estradiol); 5FS1NJ6Q8N (Nitromifene); 9007-49-2 (DNA); FB33469R8E (Estriol); S4ZLZ1K74B (triphenylethylene)
[Em] Mês de entrada:9004
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:900101
[St] Status:MEDLINE


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Fotocópia
[PMID]:2191894
[Au] Autor:Schlinger BA; Callard GV
[Ad] Endereço:Department of Psychology, University of California, Los Angeles 90024.
[Ti] Título:Aromatization mediates aggressive behavior in quail.
[So] Source:Gen Comp Endocrinol;79(1):39-53, 1990 Jul.
[Is] ISSN:0016-6480
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although testosterone (T) stimulates aggressive and reproductive behaviors in males of many vertebrate species, it is now known that the full expression of T action in the brain requires aromatization to estradiol (E2) and subsequent interaction of locally formed E2 with nuclear estrogen receptors. In experiments reported here, we used a behavioral test which quantifies the response of an individual male Japanese quail (Coturnix coturnix japonica) to the visual stimulus of a conspecific. We have called this behavior aggression because it shares many features in common with traditional measures of aggression, e.g., predicting dominance and subordinance. Nevertheless, the behavior probably also combines a complex steroid-sensitive masculine behavior. The advantage of this test is that it allows the discrimination of individual differences in masculine behavior but avoids fighting and sexual encounters per se, thereby reducing effects of learning, a problem with previous tests of avian aggression. In addition, this test has been applied usefully to identify neuroendocrine correlates to male behavior. Using this test, the arousal of reproductively inactive males (hereafter referred to as aggression) is activated by administration of T or estradiol benzoate (EB), but not by 5 alpha-dihydrotestosterone (DHT). T-induced aggression was blocked by the aromatase inhibitor 4-hydroxyandrostenedione (OHA), an effect partially reversed by treatment with EB. In addition, OHA or the estrogen receptor blocker CI-628 reduced aggressiveness of reproductively active males whereas the androgen receptor blocker flutamide had no effect. Results with the 5 alpha-reductase inhibitor N,N-diethyl-4-methyl-3-oxo-4-aza-5 alpha-androstane-17 alpha-carboxyamide (4-MA) were equivocal. Additionally, treatment of reproductively inactive quail with T or E2 but not DHT increased aromatase activity in the hypothalamus-preoptic area (HPOA). We conclude, therefore, that T to E2 conversion is essential for the activation of aggressiveness in this species. Although locally formed estrogen exerts its effects on aggression in part by increasing activity of aromatase per se, analysis of the time course of behavioral induction or suppression by the various treatments suggests that the response has multiple components, including both short latency, receptor-independent and long latency, receptor-dependent events.
[Mh] Termos MeSH primário: Agressão/fisiologia
Aromatase/metabolismo
Comportamento Animal/fisiologia
Coturnix/fisiologia
Estradiol/farmacologia
Codorniz/fisiologia
Testosterona/farmacologia
[Mh] Termos MeSH secundário: Inibidores de 5-alfa Redutase
Agressão/efeitos dos fármacos
Androstenodiona/análogos & derivados
Androstenodiona/farmacologia
Animais
Inibidores da Aromatase
Azasteroides/farmacologia
Di-Hidrotestosterona/análogos & derivados
Di-Hidrotestosterona/farmacologia
Estradiol/metabolismo
Feminino
Flutamida/farmacologia
Hipotálamo/enzimologia
Masculino
Atividade Motora/efeitos dos fármacos
Nitromifeno/farmacologia
Área Pré-Óptica/enzimologia
Testosterona/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (5-alpha Reductase Inhibitors); 0 (Aromatase Inhibitors); 0 (Azasteroids); 08J2K08A3Y (Dihydrotestosterone); 3XMK78S47O (Testosterone); 409J2J96VR (Androstenedione); 4TI98Z838E (Estradiol); 5FS1NJ6Q8N (Nitromifene); 73671-86-0 (17-N,N-diethylcarbamoyl-4-methyl-4-azaandrostane-3-one); 76W6J0943E (Flutamide); EC 1.14.14.1 (Aromatase); PUB9T8T355 (formestane)
[Em] Mês de entrada:9007
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:900701
[St] Status:MEDLINE



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