Patterson-Buckendahl Patricia, Kubovcakova Lucia, Krizanova Olga, Pohorecky Larissa A, Kvetnansky Richard
Center of Alcohol Studies, Rutgers University, 607 Allison Road, Piscataway, NJ 08854, USA.
Alcohol. 2005 Nov;37(3):157-66. doi: 10.1016/j.alcohol.2005.09.007.
Numerous reports document altered drinking behavior following acute stressors but few describe physiological responses to acute stress of chronic ethanol consuming subjects. We tested rats' responses to 120-min foot restraint immobilization (Immo) after 1 week of liquid diet containing 5% wt/vol ethanol (ethanol-fed). Controls consumed isocaloric liquid diet ad libitum (adlib-fed) or in amounts equal to that of ethanol-fed subjects on the previous day (pair-fed). Each rat was implanted with a tail artery cannula on day 7 to allow remote blood collection before and during Immo on day 8. Plasma epinephrine (Epi); norepinephrine (NE); corticosterone (Cort); prolactin (PRL); adrenomedullary gene expression of catecholamine biosynthetic enzymes tyrosine hydroxylase (TH), dopamine beta-hydroxylase (DBH), and phenylethanolamine-N-methyl transferase (PNMT); and TH protein levels were measured. Ethanol-fed rats had two to threefold higher basal plasma Epi and NE and tended to have increased Cort compared to adlib-fed or pair-fed rats. Immo increased Epi and NE in ethanol-fed rats more than twofold above those observed in controls, and also increased Cort more in ethanol-fed than in control rats. PRL was marginally affected. Ethanol potentiated the normal immobilization-induced increase in adrenomedullary TH, DBH, and PNMT messenger RNA (mRNA). TH protein increased only in ethanol-fed rats. Increased plasma catecholamine levels, adrenomedullary gene expression, and TH protein concentration in nonimmobilized ethanol-fed rats strongly suggest that ethanol consumption was itself a stressor, which potentiated the subsequent response to acute Immo. Moreover, the observed interaction of ethanol and stress on plasma catecholamine levels illustrates the importance of minimizing additional stressful stimuli when investigating ethanol's physiological effects.
众多报告记录了急性应激源后饮酒行为的改变，但很少有研究描述慢性乙醇摄入者对急性应激的生理反应。我们测试了大鼠在含5%重量/体积乙醇的液体饮食（乙醇喂养）1周后对120分钟足部束缚固定（固定）的反应。对照组自由摄食等热量液体饮食（自由摄食）或摄入量与前一天乙醇喂养组相同（配对喂养）。在第7天给每只大鼠植入尾动脉插管，以便在第8天固定前和固定期间远程采集血液。测量血浆肾上腺素（Epi）、去甲肾上腺素（NE）、皮质酮（Cort）、催乳素（PRL）、儿茶酚胺生物合成酶酪氨酸羟化酶（TH）、多巴胺β-羟化酶（DBH）和苯乙醇胺-N-甲基转移酶（PNMT）的肾上腺髓质基因表达以及TH蛋白水平。与自由摄食或配对喂养的大鼠相比，乙醇喂养的大鼠基础血浆Epi和NE高出两到三倍，且Cort有升高趋势。固定使乙醇喂养大鼠的Epi和NE增加幅度比对照组高出两倍多，且乙醇喂养大鼠的Cort增加幅度也大于对照大鼠。PRL受到的影响较小。乙醇增强了正常固定诱导的肾上腺髓质TH、DBH和PNMT信使核糖核酸（mRNA）的增加。TH蛋白仅在乙醇喂养的大鼠中增加。未固定的乙醇喂养大鼠血浆儿茶酚胺水平、肾上腺髓质基因表达和TH蛋白浓度的增加强烈表明，乙醇摄入本身就是一种应激源，它增强了随后对急性固定的反应。此外，观察到的乙醇和应激对血浆儿茶酚胺水平的相互作用说明了在研究乙醇的生理作用时尽量减少额外应激刺激的重要性。
