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The supraoptic nucleus (SON) of the hypothalamus is an important integrative brain structure that coordinates responses to perturbations in water balance and regulates maternal physiology through the release of the neuropeptide hormones vasopressin and oxytocin into the circulation. Both dehydration and lactation evoke a dramatic morphological remodeling of the SON, a process known as function-related plasticity. We hypothesize that some of the changes seen in SON remodeling are mediated by differential gene expression, and have thus used microarrays to document global changes in transcript abundance that accompany chronic dehydration in female rats, and in lactation. In situ hybridization analysis has confirmed the differential expression of three of these genes, namely TNF-induced protein 6, gonadotropin-inducible transcription factor 1, and ornithine decarboxylase antizyme inhibitor 1. Comparison of differential gene expression patterns in male and female rats subjected to dehydration and in lactating rats has enabled the identification of common elements that are significantly enriched in gene classes with particular functions. Two of these are related to the requirement for increased protein synthesis and hormone delivery in the physiologically stimulated SON (translation initiation factor activity and endoplasmic reticulum-Golgi intermediate compartment, respectively), whereas others are consistent with the concept of SON morphological plasticity (collagen fibril organization, extracellular matrix organization and biogenesis, extracellular structure organization and biogenesis, and homophilic cell adhesion). We suggest that the genes coordinately regulated in the SON as a consequence of dehydration and lactation form a network that mediates the plastic processes operational in the physiologically activated SON.
|Translated title of the contribution
|Transcriptomic analysis of the osmotic and reproductive remodeling of the female rat supraoptic nucleus
|3483 - 3491
|Number of pages
|Early online date
|26 Jul 2011
|Published - 1 Sept 2011
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