GENETICALLY-DETERMINED DIFFERENCES IN THE ANTAGONISTIC EFFECT OF PRESSURE ON ETHANOL-INDUCED LOSS OF RIGHTING REFLEX IN MICE
GENETICALLY-DETERMINED DIFFERENCES IN THE ANTAGONISTIC EFFECT OF PRESSURE ON ETHANOL-INDUCED LOSS OF RIGHTING REFLEX IN MICE
复制标题
DOI：
10.1111/j.1530-0277.1992.tb00629.x
复制
发表时间：
1992-02-01
影响因子：
3.2
通讯作者：
SYAPIN, PJ
中科院分区：
文献类型：
--
作者：
ALKANA, RL;FINN, DA;SYAPIN, PJ
高压暴露对抗乙醇的行为影响在各种各样的物种。最近的研究表明，有基因决定的差异，在酒精敏感性的体温操纵的影响，基因型也可能影响高压暴露对酒精中毒的影响。为了研究这种可能性，将注射乙醇的长睡眠（LS）/lbg（2.7 g/kg）、短睡眠（SS）/lbg（4.8 g/kg）、129/J（2.9 g/kg）和C57 BL/6 J（3.6 g/kg）小鼠暴露于一个大气压绝对（ATA）空气或暴露于一个或12个ATA氦氧（heliox），环境温度选择为抵消乙醇和氦诱导的体温过低。高压暴露显着降低LS，129，和C57小鼠翻正反射（LORR）的持续时间的损失，但在SS小鼠。第二个实验发现，高压暴露显着减少LORR持续时间和增加血液乙醇浓度（BEC）在恢复翻正反射（RORR）在LS小鼠，但没有显着影响SS小鼠的措施。这些结果表明，暴露于12 ATA氦氧混合气拮抗乙醇诱导的LORR在LS，129和C57小鼠，但不是在SS小鼠。与以前的结果，目前的研究结果表明，在LS，129，和C57小鼠的拮抗作用反映了压力诱导的大脑对乙醇的敏感性降低，SS小鼠缺乏拮抗作用不能解释压力诱导或基因型差异乙醇药代动力学。SS和LS小鼠对乙醇诱导的LORR的压力拮抗作用的不同敏感性表明，高压暴露可以用作一种工具，将这些品系在其行为和体外对乙醇的反应之间的差异联系起来，从而有助于识别中毒的关键神经化学机制。
Hyperbaric exposure antagonizes ethanol's behavioral effects in a wide variety of species. Recent studies indicating that there are genetically determined differences in the effects of body temperature manipulation on ethanol sensitivity suggested that genotype might also influence the effects of hyperbaric exposure on ethanol intoxication. To investigate this possibility, ethanol injected long sleep (LS)/lbg (2.7 g/kg), short sleep (SS)/lbg (4.8 g/kg), 129/J (2.9 g/kg), and C57BL/6J (3.6 g/kg) mice were exposed to one atmosphere absolute (ATA) air or to one or 12 ATA helium-oxygen (heliox) at ambient temperatures selected to offset ethanol and helium-induced hypothermia. Hyperbaric exposure significantly reduced loss of righting reflex (LORR) duration in LS, 129, and C57 mice, but not in SS mice. A second experiment found that hyperbaric exposure significantly reduced LORR duration and increased the blood ethanol concentration (BEC) at return of righting reflex (RORR) in LS mice, but did not significantly affect either measure in SS mice. These results indicate that exposure to 12 ATA heliox antagonizes ethanol-induced LORR in LS, 129 and C57 mice, but not in SS mice. Taken with previous results, the present findings suggest that the antagonism in LS, 129, and C57 mice reflects a pressure-induced decrease in brain sensitivity to ethanol and that the lack of antagonism in SS mice cannot be explained by pressure-induced or genotypic differences in ethanol pharmacokinetics. The differential sensitivities of SS and LS mice to pressure-antagonism of ethanol-induced LORR suggest that hyperbaric exposure can be used as a tool to link differences between these lines in their behavioral and in vitro responses to ethanol and thus may aid in the identification of critical neurochemical mechanisms that underlie intoxication.