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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neuroendocrinology 6 (1994), S. 0 
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Acute studies of GH removal by hypophysectomy or GH replacement in adult rats have shown that GH has a positive influence on its hypothalamic inhibitory hormone somatostatin (SRIH). The present study was undertaken to assess the effect of lifelong exposure to elevated GH on the development and differentiation of SRIH-producing hypothalamic neurons, including comparison of differing GH levels and heterologous species of GH. Expression of somatostatin peptide and mRNA was evaluated using respective immunocytochemistry and in situ hybridization in brains of transgenic mice bearing constructs of either human (hGH) or bovine (bGH) linked to metallothionein (MT) promoter or bGH linked to phosphoenolpyruvate carboxykinase (PEPCK) promoter. Nontransgenic littermates served as controls. All transgenic constructs resulted in high levels of circulating heterologous GH and significantly elevated body weights. Both bGH levels and body weights were higher in PEPCK-bGH than in MT-bGH mice; mean weights were not different between MT-bGH and MT-hGH mice. Numbers of SRIH-immunoreactive neurons in the hypophysiotropic periventricular nucleus (PeN) of transgenic mice showed a two-fold increase (P〈0.01) relative to control animals; the number of SRIH-positive cells in the medial basal hypothalamus (MBH) was comparable for transgenic and control mice. Total SRIH mRNA in situ hybridization intensity also showed a two-fold increase (P〈0.05) in the PeN of all transgenic mice compared with controls, and was not elevated in the MBH. The higher levels of GH produced in PEPCK-bGH transgenic mice led to greater weight gain, but not to greater SRIH expression than in other GH-transgenic mice, suggesting that the increased SRIH cell number and mRNA in the PeN of MT-GH-transgenic mice may represent a plateau of maximal feedback stimulation. The results indicate that lifelong elevated heterologous GH in mice stimulates hypothalamic SRIH expression markedly. It is not known whether this mechanism is direct or indirect via a mediator of GH such as IGF, but the heterologous GH appears to be specific to these hypophysiotropic neurons.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    American Journal of Anatomy 172 (1985), S. 307-316 
    ISSN: 0002-9106
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Ventral spinal roots at all spinal levels in humans contain many unmyelinated axons, as do all spinal roots of the cat which have been examined. Rats, however, have fewer unmyelinated fibers in cervical and certain lumbar ventral roots. To determine if unmyelinated fibers are distributed uniformly in ventral roots of the cat, cervical and lumbar ventral roots were examined by light and electron microscopy, and axons were counted. Lesions were made to determine the origin of unmyelinated fibers in ventral root L6. From 5 to 15% of the axons in cervical ventral roots are unmyelinated. This distribution of unmyelinated fibers in the cat is similar to the distribution in humans, although the cervical ventral roots of the cat contain relatively fewer unmyelinated fibers than the cervical ventral roots of humans. Approximately 24% of the axons in ventral root L6 are unmyelinated. More than 90% of these axons degenerate proximal to, but not distal to, a ventral rhizotomy and ipsilateral to a dorsal root ganglionectomy. Thus, most unmyelinated axons in ventral root L6 appear to arise from dorsal root ganglion cells. Much variation in the number and percent of unmyelinated axons in ventral roots at the same spinal level exists between individual cats and between opposite sides of the same cat.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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