| pubmed-article:18275957 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18275957 | lifeskim:mentions | umls-concept:C0700597 | lld:lifeskim |
| pubmed-article:18275957 | lifeskim:mentions | umls-concept:C0010132 | lld:lifeskim |
| pubmed-article:18275957 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:18275957 | lifeskim:mentions | umls-concept:C0205099 | lld:lifeskim |
| pubmed-article:18275957 | pubmed:issue | 2-3 | lld:pubmed |
| pubmed-article:18275957 | pubmed:dateCreated | 2008-3-21 | lld:pubmed |
| pubmed-article:18275957 | pubmed:abstractText | Corticotropin releasing factor (CRH) has been shown to contribute critically to molecular and neuroendocrine responses to stress during both adulthood and development. This peptide and its receptors are expressed in the hypothalamus, as well as in limbic brain areas including amygdala and hippocampus. This is consistent with roles for CRH in mediating the influence of stress on emotional behavior and cognitive function. The expression of CRH and of its receptors in hypothalamus, amygdala and hippocampus is age-dependent, and is modulated by stress throughout life (including the first postnatal weeks). Uniquely during development, the cardinal influence of maternal care on the central stress response governs the levels of central CRH expression, and may alter the 'set-point' of CRH-gene sensitivity to stress in a lasting manner. | lld:pubmed |
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