Dzoljic M, Erdmann W, Dzoljic M R
Department of Anaesthesiology, University of Amsterdam, The Netherlands.
Br J Anaesth. 1996 Oct;77(4):522-5. doi: 10.1093/bja/77.4.522.
We have examined the role of benzodiazepine receptors in nitrous oxide-induced neuronal depression in rats. The changes in neuronal excitability induced by nitrous oxide and the benzodiazepine inverse agonist, Ro15-4513, were monitored by measurement of visual evoked potentials (VEP). Administration of Ro15-4513 10 mg kg-1 i.p., in rats breathing air, did not affect the amplitude or latency of VEP. However, the same concentrations of Ro15-4513 antagonized nitrous oxide-induced depression of VEP amplitudes. We conclude that antagonism of nitrous oxide-induced depression by Ro15-4513 indicates that at least part of the decreased neuronal excitability caused by nitrous oxide could be ascribed to interactions with the GABAA receptor complex.
我们研究了苯二氮䓬受体在大鼠一氧化二氮诱导的神经元抑制中的作用。通过测量视觉诱发电位（VEP）来监测一氧化二氮和苯二氮䓬反向激动剂Ro15 - 4513诱导的神经元兴奋性变化。给呼吸空气的大鼠腹腔注射10 mg kg-1的Ro15 - 4513，不影响VEP的幅度或潜伏期。然而，相同浓度的Ro15 - 4513可拮抗一氧化二氮诱导的VEP幅度降低。我们得出结论，Ro15 - 4513对一氧化二氮诱导的抑制作用的拮抗表明，一氧化二氮引起的神经元兴奋性降低至少部分可归因于与GABAA受体复合物的相互作用。
