THYROXINE AND PROLACTIN EFFECT TIDA NEURON ACTIVITY

多巴胺水平、儿茶酚胺组织荧光与多巴胺生物合成 明显和选择性地缺乏斯内尔的正中隆起(ME) 和艾姆斯矮小的老鼠。儿茶酚胺，可能是DA，在体内的生物合成 Ames侏儒小鼠的下丘脑内侧基底核(MBH)也存在缺陷。 这些动物的侏儒症是由于缺乏生长激素(GH)而引起的。 和甲状腺功能减退症。此外，这些矮小的老鼠似乎没有 循环催乳素(PRL)。最近的数据表明，PRL替代 2周可增强Ames侏儒ME的DA合成，但对 正常水平。有趣的是，生长激素或甲状腺素(T4)的替代物是AS 催乳素能有效促进矮生儿茶酚胺的生物合成 MBH。总的来说，这些观察结果导致了我们的假设，即PRL 在出生后的成熟过程中起着关键的和以前没有被怀疑的作用 结节漏斗状多巴胺(TIDA)神经元通路。神经 这条通路的末端负责正常高水平的 在验尸官身上发现的。神经化学、重组DNA和 将利用形态技术来确定(1)是否存在 TIDA细胞体缺乏(2)PRL是否诱导DA的恢复 在ME中合成需要合成新的酪氨酸信使核糖核酸 羟基酶(TH)，DA合成中的限速酶，(3)如果GH或T4 具有促进DA合成的有效作用，尽管相对滞后 在侏儒ME中，(4)TIDA神经元的出生后发育 正常小鼠可被实验诱导的低催乳素血症干扰 或者是甲状腺功能减退症。 TIDA神经通路是公认的主要机制。 参与调节垂体前叶催乳素的分泌。这个 获得的结果应该为我们提供一个新的视角，了解一个独特的和以前的 反过来，PRL可能在婴儿出生后的发育过程中起到意想不到的作用 TIDA神经元通路。更广泛地说，这些结果应该会提供新的 关于前荷尔蒙一般如何作用于 下丘脑调节机制的组织与发展 它们在成体中的分泌以及这些机制的成熟可能 由于出生后荷尔蒙循环不足而受到干扰。

Dopamine (DA) levels, catecholamine histofluorescence and DA biosynthesis are markedly and selectively deficient in the median eminence (ME) of Snell and Ames dwarf mice. Catecholamine, possibly DA, biosynthesis in the mediobasal hypothalamus (MBH) is also deficient in the Ames dwarf mouse. Dwarfism in these animals is secondary to an absence of growth hormone (GH) and hypothyroidism. Further, these dwarf mice appear to have no circulating prolactin (PRL). Recent data suggests that PRL replacement for 2 weeks enhances DA synthesis in the Ames dwarf ME although not to the normal level. Interestingly, GH or thyroxine (T4) replacement was as effective as PRL in increasing catecholamine biosynthesis in the dwarf MBH. Collectively, these observations have led to our hypothesis that PRL has a critical and previously unsuspected role in the postnatal maturation of the tuberoinfundibular dopamine (TIDA) neuronal pathway. The nerve terminals of this pathway are responsible for the normally high levels of DA found in the ME. A combination of neurochemical, recombinant DNA and morphologic techniques will be utilized to determine (1) if there is a deficiency of TIDA cell bodies (2) if the PRL induced restoration of DA synthesis in the ME requires the synthesis of new mRNA for tyrosine hydroxylase (TH), the rate limiting enzyme in DA synthesis, (3) if GH or T4 have potent although comparatively delayed effects to enhance DA synthesis in the dwarf ME, (4) whether the postnatal development of the TIDA neurons in normal mice can be disrupted by experimentally induced hypoprolactinemia or hypothyroidism. The TIDA neuronal pathway is well recognized as the primary mechanism involved in regulating PRL secretion by the anterior pituitary. The results obtained should provide a new insight into a unique and previously unsuspected role PRL, in turn, may have on the postnatal development of the TIDA neuron pathway. In more general terms, the results should provide new information as to how the anterior hormones in general may act in the organization and development of the hypothalamic mechanisms which regulate their secretion in the adult and how the maturation of these mechanisms may be disrupted by postnatal deficiencies in circulating hormones.