Thesis (Ph. D.)--Michigan State University. Neuroscience Program, 2008. / Title from PDF t.p. (Proquest, viewed on Aug. 17, 2009) Includes bibliographical references (p. 114-135). Also issued in print.

Thesis (Ph. D.)--West Virginia University, 1999. / Title from document title page. Document formatted into pages; contains vi, 60 p. : ill. Includes abstract. Includes bibliographical references.

Thesis (doctoral)--Ludwig Maximilians-Universität zu München, 1979.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1970. / Typescript. Vita. Description based on print version record. Includes bibliographical references.

Proefschrift--Rijksuniversiteit te Groningen. / "Stellingen" [2] p. inserted. Includes bibliographical references.

Thesis (M.S.)--Florida State University, 2006. / Advisor: Lisa Eckel, Florida State University, College of Arts and Sciences, Dept. of Psychology. Title and description from dissertation home page (viewed June 15, 2006). Document formatted into pages; contains vi, 34 pages. Includes bibliographical references.

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Programa de Pós-Graduação em Ciências Biológicas. Núcleo de Pesquisas em Ciências Biológicas, Pró-Reitoria de Pesquisa de Pós Graduação, Universidade Federal de Ouro Preto. / Submitted by giuliana silveira (giulianagphoto@gmail.com) on 2016-04-27T17:42:30Z No. of bitstreams: 1 DISSERTAÇÃO_InfluenciaEstradiolTranstorno.pdf: 1710656 bytes, checksum: 0a1fee22586a4ac94cc3f718e0449f53 (MD5) / Approved for entry into archive by Gracilene Carvalho (gracilene@sisbin.ufop.br) on 2016-04-27T19:17:43Z (GMT) No. of bitstreams: 1 DISSERTAÇÃO_InfluenciaEstradiolTranstorno.pdf: 1710656 bytes, checksum: 0a1fee22586a4ac94cc3f718e0449f53 (MD5) / Made available in DSpace on 2016-04-27T19:17:43Z (GMT). No. of bitstreams: 1 DISSERTAÇÃO_InfluenciaEstradiolTranstorno.pdf: 1710656 bytes, checksum: 0a1fee22586a4ac94cc3f718e0449f53 (MD5) Previous issue date: 2015 / A restrição alimentar (RA) severa provoca carência energética e nutricional, levando o indivíduo à desnutrição, e este desequilíbrio acarreta inúmeras consequências bioquímicas, fisiológicas e emocionais, tais como ansiedade, pânico e danos à memória. A RA também altera o eixo hipotálamo-hipófise-ovariano, que é a via que regula a produção de hormônios ovarianos, ocasionando redução da síntese e liberação de estradiol pelos ovários. Estudos já mostraram a presença de alta densidade de receptores de estradiol do tipo β (ERβ), que quando ativados resultam em efeitos ansiolíticos, no núcleo dorsal da rafe (NDR), indicando uma relação entre o estradiol, o NDR e os transtornos de ansiedade generalizada (TAG) e pânico (TP). O NDR é uma importante estrutura encefálica relacionada a fisiopatologia dos TAG e TP. Assim, o nosso objetivo foi investigar a influência do estradiol no NDR sobre os TAG e TP em ratas submetidas à restrição alimentar. Para isso, ratas Fischer (210 ± 10g) foram divididas em controle (C) e RA e alojadas individualmente. Durante 14 dias, as C receberam ração ad libitum e os RA receberam 40% do consumo médio dos C. No 7° dia foram anestesiados com ketamina-xilazina para inserção de cânula-guia no NDR. Ao final do protocolo dietético, cada animal foi submetido a dois diferentes ensaios nos quais ou veículo (100 nL) ou estradiol (0,5 pmol/100 nL) foi microinjetado no NDR. Após 20 minutos, as ratas foram testadas no Labirinto em T Elevado (LTE), um aparato que permite avaliar comportamento de ansiedade (esquiva inibitória) e pânico (fuga), e em seguida foram colocadas no campo aberto (arena retangular que avalia a atividade locomotora do animal). No dia seguinte as ratas foram testadas novamente no LTE para avaliação da memória. Nossos resultados mostraram que as ratas RA possuíam o útero mais leve em relação às controle, sugerindo que a RA alimentar reduz a concentração de hormônios ovarianos, entre eles o estradiol. Nós também observamos que as RA levaram mais tempo para sair do braço fechado do LTE do que as C durante a esquiva (F1,63 = 10,34; p = 0,0021), o que indica um comportamento mais ansioso pelo grupo RA. Ao microinjetarmos estradiol no NDR das ratas RA, notou-se que o tempo de latência de saída do braço fechado diminuiu em relação àquelas que receberam veículo (F2,65 = 3,86; p=0,0002), sugerindo que o estradiol agiu como um agente ansiolítico revertendo o comportamento ansioso apresentado no experimento anterior. Não encontramos diferença entre os grupos no tempo de latência de fuga. Em relação à atividade locomotora, as ratas RA mostraram-se menos ativas que as C, independente da administração de veículo ou estradiol no NDR. Diante disso, sugerimos que a RA reduz os níveis de estradiol, diminuindo a concentração disponível deste XVI hormônio para atuar nos receptores presentes no NDR, o que altera o controle desta via, levando ao comportamento de ansiedade nas ratas. _________________________________________________________________________________________________________________________________________ / ABSTRACT : Food restriction (FR) causes severe energy and nutritional deficiency, leading the individual to malnutrition, and this imbalance results in countless biochemical, physiological and emotional consequences such as anxiety, panic and damage to memory. FR also alters the hypothalamic-pituitary-ovarian axis, which is the pathway that regulates the production of the ovarian hormones, leading to reduced synthesis and release of estradiol by the ovaries. Studies have shown the presence of high density estradiol β receptors (ERβ) in the dorsal raphe nucleus (DRN) indicating a relationship among estradiol, the DRN and generalized anxiety disorder (GAD) and panic disorder (PD). The DRN is an important brain structure related to the pathophysiology of GAD and PD. Thus, the aim of our study was to investigate the influence of estradiol in DRN on GAD and PD in female rats subjected to food restriction. For that, female Fischer rats (210 ± 10g) were divided into control (C) and FR and housed individually. For 14 days, the C received food ad libitum and FR received 40% of the average consumption of the C. On the 7th day the rats were anesthetized with ketamine-xylazine for insertion of the cannula guide in the DRN. At the end of the dietary protocol, each animal was subjected to two tests in which vehicle (100 nL) or estradiol (0.5 pmol / 100 nl) was microinjected in the DRN. After 20 minutes, the rats were tested in the Elevated T Maze (ETM), an apparatus designed to measure anxiety behavior (inhibitory avoidance) and panic (escape), and then were placed in the open field (rectangular arena that measures the locomotor activity). The following day the rats were retested in the ETM for the evaluation of memory. Our results show that FR had a lower weight of the rat uterus than the control, suggesting that FR reduces the concentration of ovarian hormones including estradiol. We have also found that the FR animals showed increased avoidance latences (F1,63 = 10.34, p = 0.0021), which indicates a more anxious behavior by the FR group. After the estradiol microinjetion in the DRN of FR rats, we noted that the latency to leave the closed arm decreased compared to those animals receiving vehicle (F2,65 = 3.86; p = 0.0002), suggesting that estradiol acted as an anxiolytic agent reversing the anxious behavior presented in the previous experiment. We found no difference between groups in the escape latency time. Regarding the locomotor activity of the FR rats were less active than C, regardless of vehicle or estradiol administration in the DRN Therefore, we suggest that FR reduces estradiol levels, reducing the available concentration of this hormone to act on receptors in the DRN, which changes the control of this pathway, leading to anxiety behavior in rats.

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Master of Science / Animal Sciences and Industry / Jeffrey S. Stevenson / Using an activity monitoring system (AMS) equipped with an accelerometer, 2 experiments were conducted to test the hypotheses that: (1) altering progesterone before inducing luteolysis or (2) exposing cows to estradiol cypionate (ECP) or testosterone propionate (TP) after luteolysis would increase occurrence and intensity of estrus. In experiment 1, cows (n = 154) were fitted with an AMS collar and a pressure-sensitive, rump-mounted device (HW) and assigned to 3 treatments: 1) CL only; 2) no CL + progesterone insert (CIDR); or 3) CL + 2 CIDR to achieve different concentrations of progesterone. Progesterone concentration 24 through 120 h post-treatment was greatest (P < 0.01) in CL + 2 CIDR, followed by CL, and no CL + CIDR cows. Estrus occurred 11 to 12 h earlier (P < 0.01) in no CL + CIDR compared with CL-bearing cows. Estrus intensity was greater (P < 0.05) after CL + 2 CIDR than CL only cows. The AMS and HW determined 68 and 62% of qualifying cows to be in estrus (estrus was defined: follicle ≥ 10 mm at PGF[subscript 2α] and progesterone ≤ 0.5 ng/mL 72 h later), respectively. In experiment 2, cows (n = 203) were equipped with an AMS and a friction-activated, rump-mounted patch (Estrotect patch; ET) and assigned to receive 1 mg ECP, 2 mg TP, or control 24 h after PGF[subscript 2α]. Estradiol 24 h post treatment was greater (P < 0.01) in ECP compared with controls. Estrus expression detected by ET in all cows tended (P = 0.10) to be greater for ECP compared with controls. More (P < 0.05) qualifying cows were detected in estrus after ECP compared with controls. Compared with controls and in response to ECP, estrus occurred 17 to 20 h earlier (P < 0.01) and was of greater (P < 0.05) intensity. The AMS and ET determined 71 and 74% of cows to be in estrus, respectively. Of cows exposed to the AMS, HW, or ET, 62 to 74% were detected in estrus and more than 94% subsequently ovulated. In contrast, of the residual cows not detected in estrus, 60 to 76% ovulated in the absence of detected estrus. Only ECP was successful in inducing more estrus expression and, proportions detected in estrus never exceeded 80%. Given the large proportion of cows ovulating in the absence of estrus, further research is warranted to determine if conception is achievable by inseminating cows not detected in estrus by 80 h post-PGF[subscript 2α].