Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085631 (agitation)
 12,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study investigated the effect of prenatal dexamethasone (Dex) exposure on early perinatal events, hippocampal function, and response to stress. Pregnant rats received Dex in the evening water (2.5 microg/ml) or tap water (Veh) from gestational day 15 until delivery. On the day of parturition, pups were randomized, cross-fostered, and reduced to eight or nine per dam. Four groups resulted: Veh-Veh (offspring exposed to Veh in utero, rearing mother treated with Veh during gestation), Veh-Dex, Dex-Veh, and Dex-Dex. Spatial visual memory was evaluated with the Morris water maze. The corticosterone response to restraint stress was examined, and the expression of hippocampal glucocorticoid and mineralocorticoid receptors mRNA was determined by in situ hybridization. Exposure to Dex caused restlessness in mothers, low birth weights, and poor weight gain in the offspring. The Dex-Dex males had impaired spatial learning, inability to rapidly terminate the adrenocortical response to stress, and decreased hippocampal glucocorticoid receptor (GR) mRNA expression. In contrast, Dex-exposed animals reared by Veh-treated mothers had adequate spatial learning, enhanced glucocorticoid feedback, and increased hippocampal GR mRNA. We conclude that the environment provided by a healthy mother during the postnatal period can prevent the detrimental effects of prenatal Dex administration on cognition, GR mRNA expression of the hippocampus, and the quality of the stress response.
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PMID:Effects of prenatal dexamethasone on spatial learning and response to stress is influenced by maternal factors. 1104 76

Plasma corticosterone increases during spring migration in a variety of bird species, including the Gambel's white-crowned sparrow Zonotrichia leucophrys gambelii. Corticosterone is elevated specifically in association with migratory flight, suggesting that corticosterone may promote processes such as energy mobilization and/or migratory activity. General effects of glucocorticoids support such a prediction. Because glucocorticoids exert permissive effects on food intake, corticosterone may also participate in the regulation of migratory hyperphagia. To examine the role of corticosterone during migration, we induced Gambel's white-crowned sparrows to enter the migratory condition and compared food intake and locomotor activity between controls and birds injected with RU486--an antagonist to the low-affinity glucocorticoid receptor (GR). In addition, we investigated effects of RU486 in birds that were subjected to a short-term fast. Results indicate that RU486 did not affect locomotor activity. However, consistent with its effects in mammals, RU486 suppressed food intake. Thus, hyperphagia and migratory restlessness, the two behaviors that characterize migration, may be regulated by different mechanisms. Lastly, RU486 antagonized fasting-induced lipid mobilization, as evidenced by decreased plasma free fatty acids. Thus, data on spring migrants suggest that endogenous corticosterone levels act through the GR to support hyperphagia and that the GR promotes availability of lipid fuel substrates in association with periods of energetic demand, e.g. during migratory flight.
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PMID:The low-affinity glucocorticoid receptor regulates feeding and lipid breakdown in the migratory Gambel's white-crowned sparrow Zonotrichia leucophrys gambelii. 1463 41