Literature DB >> 23765505

New insight on the molecular aspects of glucocorticoid effects in nervous system development.

R Maggi1, D Dondi, M Piccolella, L A Casulari, L Martini.   

Abstract

Adrenal glucocorticoids (Gc) are among the most significant hormones in the mammalian organisms; these steroids may reach and penetrate all tissues where they interact with cytoplasmic/nuclear receptors, through which they exert multiple and very multifaceted actions. The effects of physiological concentrations of Gc on brain functions have not been completely clarified, even though Gc are recognized to influence behavioral responses, emotions, cognitive processes and to take part in the neuroendocrine control of body homeostasis. Developmental programming effects of Gc in animal models and humans have been proposed. Actually, pre-natal stress, or exposure to high Gc levels, would somehow affect neuronal developmental events in some structure and this can lead to central nervous system altered functions, as the impairment of neuroendocrine activities, cognitive processes, sleep and mood disorders. Interestingly, it has been observed that these abnormalities may not be limited to the first directly exposed individuals but transmissible across generations. The establishment of animal models with localized pre-natal glucocorticoid receptors deficiency led to the accumulation of data on the possible roles of these hormones on development of the central and peripheral nervous system. The most recent findings on the effects of Gc on neuroblast development, with particular attention to neuronal migration, will be presented.

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Year:  2013        PMID: 23765505     DOI: 10.3275/9003

Source DB:  PubMed          Journal:  J Endocrinol Invest        ISSN: 0391-4097            Impact factor:   4.256


  51 in total

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9.  Glucocorticoid receptor-mediated expression of caldesmon regulates cell migration via the reorganization of the actin cytoskeleton.

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10.  Multigenerational programming in the glucocorticoid programmed rat is associated with generation-specific and parent of origin effects.

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2.  Krüppel-Like Factors 9 and 13 Block Axon Growth by Transcriptional Repression of Key Components of the cAMP Signaling Pathway.

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