Eckenhoff R G, Yang B J
Department of Anesthesia, University of Pennsylvania Medical Center, Philadelphia 19104, USA.
Neuroreport. 1994 Dec 30;6(1):77-80. doi: 10.1097/00001756-199412300-00021.
Because hydrostatic pressure can antagonize the behavioral effects of anesthetics in many organisms, we examined whether ethanol-induced immobility of the nematode Caenorhabditis elegans was antagonized by 100 ATA pressure. Nematode mobility was examined at pressures ranging from 1 ATA to 132 ATA, with and without increasing concentrations of ethanol (0-1 M). Pressure > 100 ATA alone inhibited movement of the nematode (EP50 = 111.5 +/- 0.6 ATA), as did increasing concentrations of ethanol (EC50 = 487 +/- 44 mM). Pressure and ethanol appeared to be additive, and not antagonistic. Because of previous results implicating glycine receptor antagonism as a mechanism of pressure reversal, and our current inability to observe significant behavioral effects of strychnine or glycine inhibition of high affinity strychnine binding, we suggest that an absence of glycine receptors in these organisms is the basis for a lack of pressure antagonism of ethanol immobility.
由于流体静压可拮抗许多生物体中麻醉剂的行为效应,我们研究了100个绝对大气压的压力是否能拮抗乙醇诱导的秀丽隐杆线虫的静止不动状态。在1个绝对大气压至132个绝对大气压的压力范围内,检测了有无不同浓度乙醇(0-1M)时线虫的活动能力。单独的压力>100个绝对大气压会抑制线虫的运动(半数有效压力=111.5±0.6个绝对大气压),乙醇浓度增加时也是如此(半数有效浓度=487±44mM)。压力和乙醇的作用似乎是相加的,而非拮抗的。鉴于先前的结果表明甘氨酸受体拮抗作用是压力逆转的一种机制,且我们目前无法观察到士的宁或甘氨酸对高亲和力士的宁结合的抑制作用产生显著的行为效应,我们认为这些生物体中缺乏甘氨酸受体是缺乏对乙醇诱导静止不动状态的压力拮抗作用的基础。