Hodges H, Green S
Department of Psychology, Institute of Psychiatry, London.
Physiol Behav. 1987;41(3):257-64. doi: 10.1016/0031-9384(87)90362-3.
Studies have shown that benzodiazepines (BZs) both disrupt discrimination and increase resistance to punishment. Using a delayed response task, we provide evidence that effects of BZs on discrimination cannot be fully explained by deficits in either short or long term memory, or by intolerance for delay of reward. A schedule with rewarded, nonrewarded (Time out: TO) and conflict components was used to investigate effects in rats of compounds active at the BZ receptor on successive discrimination and punished responding in parallel. The GABA transaminase inhibitor ethanolamine-O-sulphate exerted additive effects with chlordiazepoxide (CDP) on punished but not TO responding. Both GABA and CDP injected into the amygdala selectively increased conflict rates, but with peripheral treatment CDP also increased TO rates. Two inverse BZ agonists, CGS 8216 and FG 7142 antagonzied the anti-conflict effects of GABA and CDP, given within the amygdala or peripherally, but the increase in TO rates induced by systemic CDP was counteracted only by peripheral treatments. These compounds also reduced rates of conflict responding below baseline, consistent with anxiogenic activity. Effects of the BZ antagonist Ro 15-1788 were broadly similar to those of the inverse agonists, except that it did not antagonise the anti-conflict action of intra-amygdaloid GABA, nor significantly reduce punished responding at the single dose used. We conclude from these results that the anti-conflict effects of BZs are mediated by a GABAergic amygdaloid mechanism, but that the same mechanism is not involved in BZ effects on discrimination.
研究表明,苯二氮䓬类药物(BZs)既能干扰辨别能力,又能增强对惩罚的抵抗力。我们通过一项延迟反应任务提供证据表明,BZs对辨别能力的影响不能完全用短期或长期记忆缺陷,或对奖励延迟的不耐受来解释。采用一种包含奖励、无奖励(超时:TO)和冲突成分的实验程序,来平行研究作用于BZ受体的化合物对大鼠连续辨别和惩罚反应的影响。γ-氨基丁酸转氨酶抑制剂乙醇胺-O-硫酸盐与氯氮䓬(CDP)对惩罚反应有相加作用,但对TO反应无此作用。向杏仁核内注射γ-氨基丁酸(GABA)和CDP均能选择性增加冲突率,但外周给药时CDP也会增加TO率。两种反向BZ激动剂CGS 8216和FG 7142能拮抗杏仁核内或外周给予的GABA和CDP的抗冲突作用,但系统性给予CDP所诱导的TO率增加仅被外周给药所抵消。这些化合物还能使冲突反应率降至基线以下,这与致焦虑活性一致。BZ拮抗剂Ro 15 - 1788的作用与反向激动剂大致相似,只是它不拮抗杏仁核内注射GABA的抗冲突作用,在所使用的单剂量下也未显著降低惩罚反应。我们从这些结果得出结论,BZs的抗冲突作用是由杏仁核的GABA能机制介导的,但相同机制不参与BZs对辨别能力的影响。