4 research outputs found

    Regulation of the early development of the nervous system by growth factors

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    The nervous system of vertebrates begins as a thickening of the dorsal ectoderm early in embryogenesis which subsequently involutes to form the neural tube consisting of a single layer of epithelium (neuroepithelium); from this develops the entire central nervous sytem (CNS). Another population of cells bud off from the dorsal portion of the tube just prior to closure, the neural crest; these cells give rise to all the cells of the peripheral nervous system (PNS), and to many structures in the facial and branchial regions of the developing embryo

    Involvement of the extracellular-signal regulated kinase 1/2 signaling pathway in amylin's eating inhibitory effect

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    Peripheral amylin inhibits eating via the area postrema (AP). Because amylin activates the extracellular-signal regulated kinase 1/2 (ERK) pathway in some tissues, and because ERK1/2 phosphorylation (pERK) leads to acute neuronal responses, we postulated that it may be involved in amylin's eating inhibitory effect. Amylin-induced ERK phosphorylation (pERK) was investigated by immunohistochemistry in brain sections containing the AP. pERK-positive AP-neurons were double-stained for the calcitonin 1a/b receptor, which is part of the functional amylin-receptor. AP sections were also phenotyped using dopamine-beta-hydroxylase (DBH) as a marker of noradrenergic neurons. The effect of fourth ventricular administration of the ERK cascade blocker U0126 on amylin's eating inhibitory action was tested in feeding trials. The number of pERK-positive neurons in the AP was highest approximately 10-15 min after amylin treatment; the effect appeared to be dose-dependent (5-20 μg/kg amylin). A portion of pERK-positive neurons in the AP carried the amylin-receptor and 22% of the pERK-positive neurons were noradrenergic. Pre-treatment of rats with U0126 decreased the number of pERK-positive neurons in the AP after amylin injection. U0126 also attenuated the ability of amylin to reduce eating, at least when the animals had been fasted 24h prior to the feeding trial. Overall, our results suggest that amylin directly stimulates pERK in AP neurons in a time- and dose-dependent manner. Part of the AP neurons displaying pERK were noradrenergic. At least under fasting conditions, pERK was shown to be a necessary part in the signaling cascade mediating amylin's anorectic effect
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