ENDOCRINE REGULATION OF MATERNAL BEHAVIOR

母亲行为的内分泌调节

• 批准号: 7933507
• 负责人: ROBERT STAFFORD BRIDGES
• 金额: $ 14.14万
• 依托单位: TUFTS UNIVERSITY BOSTON
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-09-30 至 2011-09-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7933507
• 关键词: Accounting; Address; Adult; Affect; Aftercare; Animals; Behavior; Behavioral; Biochemical; Biological; Birth; Brain; Caring; Computer Systems Development; Data; Dependence; Development; Endocrine; Endocrine system; Estradiol; Event; Exposure to; Female; Fostering; Goals; Hormonal; Hormones; Infusion procedures; Investigation; Kidney; Knockout Mice; Lactation; Maintenance; Mammals; Maternal Behavior; Measures; Mediating; Modeling; Mothers; Neurobiology; Neuronal Plasticity; Opioid; Physiological; Pituitary Gland; Placental Lactogen; Play; Postpartum Period; Pregnancy; Preparation; Primates; Process; Progesterone; Prolactin; Prolactin Receptor; Rattus; Regulation; Relative (related person); Reproductive History; Research; Role; Series; Site; Staging; System; Testing; Time; Up-Regulation; base; experience; mRNA Expression; maternal aggression; neurochemistry; novel; prevent; programs; pup; relating to nervous system; reproductive; reproductive function; research study; social

The long-term goal of this project is to identify the neural and neurochemical mechanisms underlying the regulation of maternal behavior and to elucidate potentially novel mechanisms of neural plasticity associated with the expression of maternal behavior in the adult mammal. The specific hypothesis that will be tested is that the induction, maintenance, and retention of maternal care are under endocrine regulation by a neural lactogenic system, a system that displays significant plasticity as a function of reproductive experience. The first series of studies will examine the role of the neural prolactin (PRL) receptor in the initiation of maternal behavior. Using a rat model, we will determine whether placental lactogens, like PRL, act via the PRL receptor to stimulate the onset of behavior. A second study will use the novel PRL receptor antagonist, S179D-PRL, which will be administered centrally to test the hypothesis that activation of the PRL receptor by lactogenic hormones around the time of birth is essential for the normal onset of maternal care. The third study using ISHH will measure how pregnancy concentrations of progesterone (P) and estradiol affect expression of mRNA for neural PRL receptors. Then, central sites of P action will be examined to see how P affects the onset of maternal care and to delineate a mechanism of P's action in the initiation of maternal behavior. A second series of experiments will determine the involvement of the endocrine system in ongoing maternal care. First, the effects of exposure to PRL-secreting ectopic pituitary grafts on pup- directed maternal care and maternal aggression will be measured. Then, the effects of central administration of the PRL receptor antagonist, S179D-PRL, will be examined in lactating rats. The third set of experiments will delineate the role of the endocrine system in the retention of maternal behavior. The involvement of PRL in the opioid-mediated establishment of the retention of maternal behavior will be assessed. Finally, the effects of prior maternal experience on activation of the neural lactogenic system will be measured to see whether prior maternal experience up-regulates the brain PRL system and makes the female more sensitive to her own neural hormones. The results of these investigations will delineate common endocrine and neurochemical regulators of maternal care in mammals, present a new model for examining neuroplasticity in the adult female, and provide a basis for evaluating the effects of endocrine and neurochemical imbalances on mother-young interactions.

该项目的长期目标是确定该项目的神经和神经化学机制 调节孕产妇行为并阐明与该神经可塑性的潜在新机制 成人哺乳动物中母性行为的表达。将要测试的具体假设是诱导， 维持和保留产妇护理受神经乳酸系统的内分泌调节，一个系统 这表现出显着的可塑性，这是生殖体验的函数。第一个研究将研究 神经催乳素（PRL）受体在孕产妇行为的启动中的作用。使用大鼠模型，我们将 确定像PRL这样的胎盘泌乳素是否通过PRL受体起作用以刺激行为的发作。一个 第二项研究将使用新型的PRL受体拮抗剂S179D-PRL，该拮抗剂将集中施用以测试 假设在出生时期通过乳脂激素激活PRL受体是必不可少的 孕产妇护理的正常发作。第三项使用ISHH的研究将衡量如何妊娠浓度 孕酮（P）和雌二醇会影响神经PRL受体的mRNA表达。然后，P动作的中央站点 将检查以查看P如何影响孕产妇护理的开始并描述P在 孕产妇行为的启动。第二系列实验将确定内分泌的参与 正在进行的母亲护理中的系统。首先，暴露于PRL分泌异位垂体移植物对幼犬的影响 将测量定向的母亲护理和孕产妇侵略。然后，中央给药的影响 PRL受体拮抗剂S179D-PRL将在泌乳大鼠中检查。第三组实验将描绘 内分泌系统在孕产妇行为的保留中的作用。 PRL参与阿片类药物介导的 将评估产妇行为的保留。最后，先前的母亲经验的影响 在激活神经泌乳系统时，将测量以查看先前的母亲经验是否在上调 脑PRL系统，使女性对自己的神经激素更加敏感。这些结果 调查将描绘哺乳动物中母体护理的常见内分泌和神经化学调节剂， 研究成年女性神经可塑性的新模型，并为评估的影响提供了基础 母亲互动的内分泌和神经化学失衡。

项目成果

Hormonal regulation of maternal behavior in rats: stimulation following treatment with ectopic pituitary grafts plus progesterone.

大鼠母性行为的激素调节：异位垂体移植物加黄体酮治疗后的刺激。

• DOI: 10.1095/biolreprod37.3.518
• 发表时间: 1987
• 期刊: Biology of reproduction
• 影响因子: 3.6
• 作者: Bridges,RS;Dunckel,PT
• 通讯作者: Dunckel,PT

Central lactogenic regulation of maternal behavior in rats: steroid dependence, hormone specificity, and behavioral potencies of rat prolactin and rat placental lactogen I.

大鼠母体行为的中枢催乳调节：类固醇依赖性、激素特异性以及大鼠催乳素和大鼠胎盘催乳素 I 的行为效力。

• DOI: 10.1210/endo.138.2.4921
• 发表时间: 1997
• 期刊: Endocrinology.
• 作者: Bridges,RS;Robertson,MC;Shiu,RP;Sturgis,JD;Henriquez,BM;Mann,PE
• 通讯作者: Mann,PE

Prenatal stress reduces estradiol-induced prolactin release in male and female rats.

产前应激会减少雄性和雌性大鼠中雌二醇诱导的催乳素释放。

• DOI: 10.1016/0031-9384(87)90112-0
• 发表时间: 1987
• 期刊: Physiology & behavior
• 影响因子: 2.9
• 作者: Kinsley,CH;Bridges,RS
• 通讯作者: Bridges,RS

Hypothalamic involvement in the regulation of maternal behaviour in the rat: inhibitory roles for the ventromedial hypothalamus and the dorsal/anterior hypothalamic areas.

下丘脑参与大鼠母性行为的调节：对下丘脑腹内侧和下丘脑背侧/前部区域的抑制作用。

• DOI: 10.1046/j.1365-2826.1999.00322.x
• 发表时间: 1999
• 期刊: Journal of neuroendocrinology
• 影响因子: 3.2
• 作者: Bridges,RS;Mann,PE;Coppeta,JS
• 通讯作者: Coppeta,JS

Enhanced maternal aggression and associated changes in neuropeptide gene expression in multiparous rats.

• DOI: 10.1037/a0016734
• 发表时间: 2009-10
• 期刊: BEHAVIORAL NEUROSCIENCE
• 影响因子: 1.9
• 作者: Nephew, Benjamin C.;Bridges, Robert S.;Lovelock, Dennis F.;Byrnes, Elizabeth M.
• 通讯作者: Byrnes, Elizabeth M.