Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One-day-old chicks were individually assessed on their latency to peck pebbles, and categorized as low latency (LL) or high latency (HL) according to fear. Interactions between acute stress and systemic insulin and epinephrine on GABA(A) receptor density in the forebrain were studied. At 10 days of life, LL and HL chicks were intraperitoneally injected with insulin, epinephrine or saline, and immediately after stressed by partial water immersion for 15 min and killed by decapitation. Forebrains were dissected and the GABA(A) receptor density was measured ex vivo by the (3)[H]-flunitrazepam binding assay in synaptosomes. In non-stressed chicks, insulin (non-hypoglycemic dose) at 2.50 IU/kg of body weight incremented the Bmax by 40.53% in the HL chicks compared to saline group whereas no significant differences were observed between individuals in the LL subpopulation. Additionally, insulin increased the Bmax (23.48%) in the HL group with respect to the LL ones, indicating that the insulin responses were different according to the anxiety of each category. Epinephrine administration (0.25 and 0.50mg/kg) incremented the Bmax in non-stressed chicks, in the LL group by about 37% and 33%, respectively, compared to ones injected with saline. In the stressed chicks, 0.25mg/kg bw epinephrine increased the Bmax significantly in the HL group by about 24% compared to saline, suggesting that the effect of epinephrine was only observed in the HL group under acute stress conditions. Similarly, the same epinephrine doses co-administered with insulin increased the receptor density in both subpopulations and also showed that the highest dose of epinephrine did not further increase the maximum density of GABA(A)R in HL chicks. These results suggest that systemic epinephrine, perhaps by evoking central norepinephrine release, modulated the increase in the forebrain GABA(A) receptor recruitment induced by both insulin and stress in different ways depending on the subpopulation fearfulness.
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PMID:Recruitment of GABA(A) receptors and fearfulness in chicks: modulation by systemic insulin and/or epinephrine. 2329 Sep 33

Common variants in serotonin and corticosteroid receptor genes influence human stress in laboratory settings. Little is known of their combined effects, especially in high stress environments. This study evaluated distinct and combined effects of polymorphisms in the serotonin transporter (5HTTLPRL/S), glucocorticoid receptor (Bcl1C/G), and mineralocorticoid (-2C/G) receptor genes on adrenocortical and cardiovascular responses to intense, realistic stress. One hundred and forty four healthy, active-duty military men were studied before, during, and 24h after a stressful 12-day survival course. Dependent variables were cortisol, heart rate (HR), systolic blood pressure (SBP), and diastolic blood pressure (DBP). 5HTTLPR SS carriers revealed higher overall cortisol concentrations than L carriers (p=.022). 5HTTLPR L carriers demonstrated higher stress-induced HR than non-carriers (SS) yet rebounded to a lower recovery value (p=.026), while Bcl1 G carriers showed higher mean stress-induced HR than non-carriers (CC) (p=.047). For DBP, 5HTTLPR S carriers showed higher overall values than non-carriers (LL) (p=.043), Bcl1 GG were higher than C carriers (p=.039), and -2C/G G carriers exceeded non-carriers (CC) (p=.028). A "high" composite genotype group revealed substantially higher overall cortisol concentrations than a "low" composite genotype group (p<.001), as was the case for DBP (p=.037). This study revealed a synergistic effect of common polymorphisms on the acute stress response in healthy men. Pending additional study, these findings may have implications for drug discovery, gene therapy, and stress inoculation strategies.
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PMID:Genetic variants in serotonin and corticosteroid systems modulate neuroendocrine and cardiovascular responses to intense stress. 2482 3